Journal articles: 'Angiogenic cells'

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Sadagopan, Sathish, Neelam Sharma-Walia, Mohanan Valiya Veettil, Virginie Bottero, Rita Levine, Richard J. Vart, and Bala Chandran. "Kaposi's Sarcoma-Associated Herpesvirus Upregulates Angiogenin during Infection of Human Dermal Microvascular Endothelial Cells, Which Induces 45S rRNA Synthesis, Antiapoptosis, Cell Proliferation, Migration, and Angiogenesis." Journal of Virology 83, no. 7 (January 21, 2009): 3342–64. http://dx.doi.org/10.1128/jvi.02052-08.

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ABSTRACT Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is associated with the angioproliferative KS lesions characterized by spindle-shaped endothelial cells, inflammatory cells, cytokines, growth factors, and angiogenic factors. De novo KSHV infection of human microvascular dermal endothelial cells results in increased secretion of several growth factors, cytokines, chemokines, and angiogenic factors, and the multifunctional angiogenic protein angiogenin is one of them. KS tissue sections were positive for angiogenin, highlighting the importance of angiogenin in KS pathogenesis. Examination of KSHV-mediated angiogenin upregulation and secretion and potential outcomes revealed that during infection of primary endothelial cells, KSHV induced a time- and dose-dependent increase in angiogenin gene expression and protein secretion beginning as early as 8 h postinfection and lasting until the fifth day of our observation period. TIVE latently transformed cells (TIVE-LTC) latently infected with KSHV secreted high levels of angiogenin. Angiogenin was also detected in BCBL-1 cells (human B cells) carrying KSHV in a latent state. Significant induction of angiogenin was observed in cells expressing KSHV ORF73 (LANA-1; latent) and ORF74 (lytic) genes alone, and moderate induction was seen with the lytic KSHV ORF50 gene. Angiogenin bound to surface actin, internalized in a microtubule-independent manner, and translocated into the nucleus and nucleolus of infected cells. In addition, it increased 45S rRNA gene transcription, antiapoptosis, and proliferation of infected cells, thus demonstrating the multifunctional nature of KSHV-induced angiogenin. These activities were dependent on angiogenin nuclear translocation, which was inhibited by neomycin. Upregulation of angiogenin led to increased activation of urokinase plasminogen activator and generation of active plasmin, which facilitated the migration of endothelial cells toward chemoattractants, including angiogenin, and chemotaxis was prevented by the inhibition of angiogenin nuclear translocation. Treatment of KSHV-infected cell supernatants with antiangiogenin antibodies significantly inhibited endothelial tube formation, and inhibition of nuclear translocation of angiogenin also blocked the expression of KSHV-induced vascular endothelial growth factor C. Collectively, these results strongly suggest that by increasing infected endothelial cell 45S rRNA synthesis, proliferation, migration, and angiogenesis, KSHV-induced angiogenin could be playing a pivotal role in the pathogenesis of KSHV infection, including a contribution to the angioproliferative nature of KS lesions. Our studies suggested that LANA-1 and vGPCR play roles in KSHV-induced angiogenesis and that the angiogenic potential of vGPCR might also be due to its ability to induce angiogenin.

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Jones, Brielle, Chaoyang Li, Min Sung Park, Anne Lerch, Vimal Jacob, Nicholas Johnson, Jin-Qiang Kuang, Sandeep Dhall, and Malathi Sathyamoorthy. "Comprehensive Comparison of Amnion Stromal Cells and Chorion Stromal Cells by RNA-Seq." International Journal of Molecular Sciences 22, no. 4 (February 14, 2021): 1901. http://dx.doi.org/10.3390/ijms22041901.

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Mesenchymal stromal cells derived from the fetal placenta, composed of an amnion membrane, chorion membrane, and umbilical cord, have emerged as promising sources for regenerative medicine. Here, we used next-generation sequencing technology to comprehensively compare amniotic stromal cells (ASCs) with chorionic stromal cells (CSCs) at the molecular and signaling levels. Principal component analysis showed a clear dichotomy of gene expression profiles between ASCs and CSCs. Unsupervised hierarchical clustering confirmed that the biological repeats of ASCs and CSCs were able to respectively group together. Supervised analysis identified differentially expressed genes, such as LMO3, HOXA11, and HOXA13, and differentially expressed isoforms, such as CXCL6 and HGF. Gene Ontology (GO) analysis showed that the GO terms of the extracellular matrix, angiogenesis, and cell adhesion were significantly enriched in CSCs. We further explored the factors associated with inflammation and angiogenesis using a multiplex assay. In comparison with ASCs, CSCs secreted higher levels of angiogenic factors, including angiogenin, VEGFA, HGF, and bFGF. The results of a tube formation assay proved that CSCs exhibited a strong angiogenic function. However, ASCs secreted two-fold more of an anti-inflammatory factor, TSG-6, than CSCs. In conclusion, our study demonstrated the differential gene expression patterns between ASCs and CSCs. CSCs have superior angiogenic potential, whereas ASCs exhibit increased anti-inflammatory properties.

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Suku, Meenakshi, Ashang Luwang Laiva, Fergal J. O’Brien, and Michael B. Keogh. "Anti-Ageing Protein β-Klotho Rejuvenates Diabetic Stem Cells for Improved Gene-Activated Scaffold Based Wound Healing." Journal of Personalized Medicine 11, no. 1 (December 22, 2020): 4. http://dx.doi.org/10.3390/jpm11010004.

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Skin wounds can lead to serious morbidity complications in diabetic patients due to the reduced healing potential of autologous stem cells. One reason for the low functional potency of stem cells from diabetic patients (diabetic stem cells) is attributed to their senescent-like nature. Here, we investigated if an anti-ageing protein, β-klotho, could be used to rejuvenate diabetic stem cells and to promote pro-angiogenic gene-activated scaffold (GAS)-induced functional response for wound healing applications. Human stem cells derived from the adipose tissue (adipose-derived stem cells (ADSCs)) of normal and diabetic (type 2) donors were used for the study. We report that the β-klotho priming facilitated inflammatory signal pruning by reducing interleukin-8 release by more than half while concurrently doubling the release of monocyte chemoattractant protein-1. Additionally, β-klotho priming enhanced the pro-angiogenic response of diabetic ADSCs on GAS by dampening the release of anti-angiogenic factors (i.e., pigment epithelium-derived factor, tissue inhibitor of metalloproteinase-1 and thrombospondin-1) while simultaneously supporting the expression of pro-angiogenic factors (i.e., Vascular Endothelial Growth Factor (VEGF), angiopoietin-2 and angiogenin). Finally, we show that β-klotho pre-treatment expedites the cellular expression of matrix proteins such as collagen IV and collagen VI, which are implicated in tissue maturation. Taken together, our study provides evidence that the synergistic effect of the pro-angiogenic GAS and β-klotho activation effectively accelerates the functional development of diabetic ADSCs for wound healing applications.

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Asosingh, Kewal, Hendrik De Raeve, Mark de Ridder, Guy A. Storme, Angelo Willems, Ivan Van Riet, Benjamin Van Camp, and Karin Vanderkerken. "Role of the Hypoxic Bone Marrow Microenvironment in Multiple Myeloma Tumor Progression." Blood 104, no. 11 (November 16, 2004): 2348. http://dx.doi.org/10.1182/blood.v104.11.2348.2348.

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Abstract Recently we reported that pre-clinical myeloma disease progression in the 5T2MM mouse model is characterized by predominant CD45+ MM-cells in the early, pre-angiogenic stage stage of slow tumor progression, followed by expansion of CD45− MM-cells during the subsequent angiogenic stage of progressive tumor growth. Unlike other cancer cells, multiple myeloma (MM) cells have to survive and to grow in a microenvironment which is already hypoxic by nature. This hypoxic bone marrow (BM) microenvironment is essential for normal hematopoiesis. However, the role of BM hypoxia in myeloma tumor progression is not known. Herein we addressed this topic in the 5T2MM mouse model. Flow cytometric analysis of control mice and 5T2MM diseased mice injected with pimonidazole hypoxyprobe indicated that both normal BM and myeloma infiltrated BM are hypoxic. However, in myelomatous BM the hypoxia was significantly decreased. Analysis of HIF-1a expression, a surrogate marker of hypoxia, by flow cytometry also demonstrated significantly lower levels of hypoxia in myeloma infiltrated BM. HIF-1a expression was found in 5T2MM-cells and was significantly higher compared to the non-tumor cell fraction. In vitro culturing of 5T2MM cells under hypoxic conditions, indicated increased activation of apoptosis inducing caspase-3 in the CD45− MM-fraction, but not in the CD45+ 5T2MM-cells, suggesting that native BM hypoxia selects the tumor population for tumor initiating CD45+ 5T2MM-cells. Although angiogeneic switch and angiogeneic heterogeneity has been reported in MM, the role of myeloma associated angiogensis is remains unclear. The decreased hypoxia in myeloma infiltrated BM adds strength to the hypothesis that myeloma associated neovascularization is functional by increasing BM oxygenation. The data also suggest that the angiogenesis allows expansion of CD45− 5T2MM-cells by decreasing BM hypoxia. All together, these findings suggest an important role of BM hypoxia in myeloma tumor progression.

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Fett, James W., Daniel J. Strydom, Roy R. Lobb, Edward M. Alderman, J. Lemuel Bethune, James F. Riordan, and Bert L. Vallee. "Isolation and characterization of angiogenin, an angiogenic protein from human carcinoma cells." Biochemistry 24, no. 20 (September 1985): 5480–86. http://dx.doi.org/10.1021/bi00341a030.

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Paul, Santanu, Steven L. Allen, Kanti R. Rai, and Nicholas Chiorazzi. "Expression of Angiogenin in Normal B Lymphocytes and B-CLL Cells." Blood 106, no. 11 (November 16, 2005): 1188. http://dx.doi.org/10.1182/blood.v106.11.1188.1188.

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Abstract Angiogenesis is critical for the clinical progression of hematopoietic malignancies and depends on a series of angiogenic factors. Angiogenin is a potent angiogenic factor produced by the host microenvironment and certain neoplastic cells. The association between angiogenin, cancer progression and poor outcome in solid tumors has been documented, but its significance in B-CLL has not been defined. A previous study suggests that B-CLL patients in Rai stage O with higher angiogenin levels have a better clinical outcome. This is surprising in light of the association of angiogenin levels with progression in solid tumors. Therefore we analyzed angiogenin mRNA and protein expression by the leukemic cells of B-CLL patients in order to correlate the production of this molecule with disease progression in B-CLL. Angiogenin was expressed in B-CLL cells as well as in B cells of normal donors, although the expression in the former was much higher than in the latter. Q PCR revealed a 7-fold induction in angiogenin-specific mRNA transcription in B-CLL cells (n=10) in comparison to normal B cells (n=13). In addition, angiogenin protein was identified by confocal microscopy both within and on the cell surface of B-CLL cells. All B-CLL cases, regardless of IgV gene mutation status, express angiogenin as defined by FACS. Approximately 85% of the cells that comprise B-CLL clones (n=28) display angiogenin on their surface membranes (range: 55-98%). Furthermore approximately 13% of polyclonal B cells from normal subjects (n=12) also produce angiogenin (range: 1–33%). Using enzyme immunoassay, we also measured serum angiogenin levels and detected significant differences in 66 B-CLL patients (median: 381 ng/mL; range: 185–875) versus 24 age- and sex-matched healthy controls (median: 301 ng/mL; range: 192–536) (P = 0.0056). Surprisingly, there was no correlation between surface and serum angiogenin levels and the different V gene-defined B-CLL subgroups. Our results show for the first time that a small fraction of normal B cells and all cases of B-CLL express angiogenin transcripts as well as intracellular and surface membrane protein. Angiogenin levels do not correlate with IgV gene mutations status or expression of surface membrane CD38. The role of angiogenin in the pathogenesis and progression of B-CLL needs further study.

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Komici, Klara, Isabella Gnemmi, Claudia Sangiorgi, Fabio Luigi Massimo Ricciardolo, Mauro Rinaldi, Antonino Di Stefano, and Ermanno Eleuteri. "Indexes of Angiogenic Activation in Myocardial Samples of Patients with Advanced Chronic Heart Failure." Medicina 55, no. 12 (November 29, 2019): 766. http://dx.doi.org/10.3390/medicina55120766.

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Background and objectives: Ischemic and idiopathic heart failure are characterized by reactive cardiac fibrosis and impaired vasculogenesis involving pro-angiogenic factors such as angiogenin, angiopoietin-1 (Ang-1), and angiopoietin-2 (Ang-2), as demonstrated in experimental models of heart failure. However, differences in the molecular pathways between these cardiomyopathies are still unclear. In this short communication, we evaluate and compare the expression of pro-angiogenic molecules in the heart tissue of patients with advanced chronic heart failure (CHF) of ischemic vs. nonischemic etiology. Materials and Methods: We obtained heart tissue at transplantation from left ventricular walls of 16 explanted native hearts affected by either ischemic (ICM) or nonischemic dilated cardiomyopathy (NIDCM). Tissue samples were examined using immunohistochemistry for angiogenic molecules. Results: We found immunopositivity (I-pos) for angiopoietin-1 mainly in the cardiomyocytes, while we observed I-pos for Ang-2 and Tie-2 receptor mainly in endothelial cells. Expression of Procollagen-I (PICP), angiogenin, Ang-1, and Tie-2 receptor was similar in ICM and NIDCM. In contrast, endothelial immunopositivity for Ang-2 was higher in ICM samples than NIDCM (p = 0.03). Conclusions: In our series of CHF heart samples, distribution of Ang-1 and angiogenin was higher in cardiomyocytes while that of Ang-2 was higher in endothelial cells; moreover, Ang-2 expression was higher in ICS than NIDCM. Despite the small series examined, these findings suggest different patterns of angiogenic stimulation in ICM and NIDCM, or at least a more altered endothelial integrity in ICD. Our data may contribute to a better understanding of the angiogenesis signaling pathways in CHF. Further studies should investigate differences in the biochemical processes leading to heart failure.

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Schanz, Andrea, Margarete Lukosz, Alexandra P. Hess, Dunja M. Baston-Büst, Jan S. Krüssel, and Christian Heiss. "hCG stimulates angiogenic signals in lymphatic endothelial and circulating angiogenic cells." Journal of Reproductive Immunology 110 (August 2015): 102–8. http://dx.doi.org/10.1016/j.jri.2015.01.011.

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Bretschneider, Henriette, Mandy Quade, Anja Lode, Michael Gelinsky, Stefan Rammelt, Stefan Zwingenberger, Klaus-Dieter Schaser, and Corina Vater. "Characterization of Naturally Occurring Bioactive Factor Mixtures for Bone Regeneration." International Journal of Molecular Sciences 21, no. 4 (February 19, 2020): 1412. http://dx.doi.org/10.3390/ijms21041412.

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In this study, the bone-regenerative potential of bioactive factors derived from adipose tissue, platelet-rich plasma (PRP) and conditioned medium from hypoxia-treated human telomerase immortalized bone-marrow-derived mesenchymal stem cells (hTERT-MSC) was investigated in vitro with the aim to develop cost-effective and efficient bone substitutes for optimized regeneration of bone defects. Adipose tissue was harvested from human donors undergoing reconstructive surgery, and adipose tissue extract (ATE) was prepared. Platelet lysates (PL) were produced by repeated freeze-thaw cycles of PRP, and hypoxia-conditioned medium (HCM) was obtained by culturing human telomerase immortalized bone-marrow-derived mesenchymal stromal cells for 5 days with 1% O2. Besides analysis by cytokine and angiogenesis arrays, ELISA was performed. Angiogenic potential was investigated in cocultures of bone-marrow-derived (BM)-MSC and human umbilical vein endothelial cells. Multiple angiogenic proteins and cytokines were detected in all growth factor mixtures. HCM and ATE contained high amounts of angiogenin and CCL2/MCP-1, whereas PL contained high amounts of IGFBP-1. Culturing cells with HCM and ATE significantly increased specific ALP activity of BM-MSC as well as tubule length and junctions of endothelial networks, indicating osteogenic and angiogenic stimulation. To achieve a synergism between chemoattractive potential and osteogenic and angiogenic differentiation capacity, a combination of different growth factors appears promising for potential clinical applications.

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Golat, Brian T., and Don F. Cameron. "Sertoli Cells Enhance Formation of Capillary-Like Structures in Vitro." Cell Transplantation 17, no. 10-11 (October 2008): 1135–44. http://dx.doi.org/10.3727/096368908787236512.

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Sertoli cells isolated from the testis (referred to as extratesticular Sertoli cells) have been shown to facilitate allo- and xenogeneic cell transplantations. It appears likely that the ability of these cells to enhance the success of cell engraftment is due, in part, to the retention of their intratesticular functions of trophic support and immunoprotection. Sertoli cells also are involved in the regulation of angiogenesis in the testis, which may also contribute to enhanced cell engraftment success facilitated by extratesticular Sertoli cells. Because the maintenance of the cell's intratesticular angiogenic function has not yet been evaluated for extratesticular Sertoli cells, this study examined the cell's ability to enhance angiogenesis in vitro. Sertoli cell conditioned media were derived from isolated rat Sertoli cell cultures and used in a rat aortic model of induced angiogenesis, in endothelial and smooth muscle cell monocultures, and in endothelial smooth muscle cocultures. An angiogenic rat cytokine array identified angiogenic factors in the control and conditioned media. Aorta sections incubated with Sertoli cell conditioned media showed a marked increase in the formation of capillary-like structures when compared to controls. Likewise, endothelial cells incubated in conditioned media organized into capillary-like structures not observed when incubated in control media. In coculture, smooth muscle cells were associated with endothelial cell-derived capillary-like structures only when incubated in conditioned media. Cytokine arrays indicated the presence and a qualitative increase of specific angiogenic growth factors in Sertoli cell conditioned media not observed in control media. Results indicate that extratesticular Sertoli cells retain their intratesticular angiogenic function in vitro.

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Anagnostopoulos, Athanasios, Evangelos Terpos, Efstathios Kastritis, Aristotelis Bamias, Konstantinos Tsionos, and Meletios A. Dimopoulos. "Angiogenic Cytokines Are Increased in the Serum of Patients with Waldenstrom’s Macroglobulinemia: Correlations with Clinical Data." Blood 106, no. 11 (November 16, 2005): 2504. http://dx.doi.org/10.1182/blood.v106.11.2504.2504.

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Abstract Angiogenesis represents an essential step of disease progression in several hematologic malignancies including multiple myeloma (MM). Bone marrow angiogenesis, assessed by microvessel density (MVD), is increased in 30% of patients with Waldenstrom’s macroglobulinemia (WM) and showed only weak correlation with bone marrow infiltration. The orchestration of two major classes of angiogenic factors, namely the vascular endothelial growth factor (VEGF) and angiopoietin-2 (Ang-2), has been shown to play a pivotal role in tumor angiogenesis. Angiogenin is a member of the ribonuclease superfamily, which participates in angiogenesis by influencing the migration and proliferation of endothelial cells, while basic fibroblast growth factor (bFGF) is another cytokine with angiogenic properties which is produced by stromal cells and plays a significant role in the pathogenesis of MM. The aim of this study was the evaluation of angiogenesis, as assessed by the measurement of the above mentioned angiogenic cytokines, in patients with WM and its correlation with clinical data of the patients. We studied 53 serum samples of 38 patients with WM (26M/12F; median age: 74 years, range: 39–85 years) in different phases of their disease. Thirteen patients were evaluated prior any kind of treatment, while 24 patients were studied during an active phase of their disease and 12 patients during remission. Furthermore, 4 patients with IgM MGUS were also studied. VEGF, angiogenin, Ang-2 and bFGF were measured using an ELISA method (R&D Systems, Minneapolis, MN, USA). In all patients, we also evaluated hemoglobin, platelet count, β2-microglobulin, and albumin levels as well as the presence of splenomegaly, hepatomegaly and lymphadenopathy at the time of sample collection. The angiogenic cytokines were also measured in 20 gender- and age-matched controls. WM patients had increased serum levels of all angiogenic cytokines compared with controls: mean ± SD for VEGF was 231 ± 168 vs. 59.2 ± 37.2 pg/ml in patients and controls, respectively (p<0.0001); for angiogenin 412.2 ± 191.3 ng/ml vs. 230.9 ± 18.9 ng/ml (p<0.0001); for Ang-2 2766 ± 917 vs. 1372 ± 541 pg/ml (p<0.0001) and for bFGF 10.6 ± 10.6 vs. 0 pg/ml (p<0.0001). Patients with IgM MGUS had also elevated values of VEGF, Ang-2, and bFGF (p<0.001), but not of angiogenin compared with controls. Untreated WM patients had increased levels of angiogenin compared with patients at remission (mean ± SD: 547.6 ± 49.4 vs. 333 ±126.8 ng/ml; p=0.01). At the time of samples collection, 9 patients had anemia (Hb<10 g/dl), while 11 patients had increased levels of β2-microglobulina (>3.5 mg/l), and 7 patients had reduced albumin levels (<3.5 g/dl). VEGF serum levels correlated with β2-microglobulin (r=0.4, p=0.012), while angiogenin levels correlated with serum albumin (r=−0.307, p=0.031). This ongoing study suggests that angiogenic cytokines are increased in patients with WM supporting a possible paracrine role of these molecules. Our results, if confirmed, may provide the basis for clinical trials in WM, which involve anti-angiogenic agents.

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Liu, Zhiping, Jiean Xu, Qian Ma, Xiaoyu Zhang, Qiuhua Yang, Lina Wang, Yapeng Cao, et al. "Glycolysis links reciprocal activation of myeloid cells and endothelial cells in the retinal angiogenic niche." Science Translational Medicine 12, no. 555 (August 5, 2020): eaay1371. http://dx.doi.org/10.1126/scitranslmed.aay1371.

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The coordination of metabolic signals among different cellular components in pathological retinal angiogenesis is poorly understood. Here, we showed that in the pathological angiogenic vascular niche, retinal myeloid cells, particularly macrophages/microglia that are spatially adjacent to endothelial cells (ECs), are highly glycolytic. We refer to these macrophages/microglia that exhibit a unique angiogenic phenotype with increased expression of both M1 and M2 markers and enhanced production of both proinflammatory and proangiogenic cytokines as pathological retinal angiogenesis–associated glycolytic macrophages/microglia (PRAGMs). The phenotype of PRAGMs was recapitulated in bone marrow–derived macrophages or retinal microglia stimulated by lactate that was produced by hypoxic retinal ECs. Knockout of 6-phosphofructo-2-kinase/fructose-2, 6-bisphosphatase (PFKFB3; Pfkfb3 for rodents), a glycolytic activator in myeloid cells, impaired the ability of macrophages/microglia to acquire an angiogenic phenotype, rendering them unable to promote EC proliferation and sprouting and pathological neovascularization in a mouse model of oxygen-induced proliferative retinopathy. Mechanistically, hyperglycolytic macrophages/microglia produced large amount of acetyl–coenzyme A, leading to histone acetylation and PRAGM-related gene induction, thus reprogramming macrophages/microglia into an angiogenic phenotype. These findings reveal a critical role of glycolytic metabolites as initiators of reciprocal activation of macrophages/microglia and ECs in the retinal angiogenic niche and suggest that strategies targeting the metabolic communication between these cell types may be efficacious in the treatment of pathological retinal angiogenesis.

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Okumo, Takayuki, Atsuko Furuta, Tarou Kimura, Kanako Yusa, Kazuhito Asano, and Masataka Sunagawa. "Inhibition of Angiogenic Factor Productions by Quercetin In Vitro and In Vivo." Medicines 8, no. 5 (May 12, 2021): 22. http://dx.doi.org/10.3390/medicines8050022.

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Background: Angiogenesis is well known to be an important event in the tissue remodeling observed in allergic diseases. Although there is much evidence that quercetin, one of the most abundant dietary flavonoids, exerts anti-allergic effects in both human and experimental animal models of allergic diseases, the action of quercetin on angiogenesis has not been defined. Therefore, in this study, we first examined the action of quercetin on the secretion of angiogenic factors from murine mast cells in vitro. We also examined the action of quercetin on angiogenic factor secretion in the murine allergic rhinitis model in vivo. Methods: Mast cells (1 × 105 cells/mL) sensitized with ovalbumin (OVA)-specific murine IgE were stimulated with 10.0 ng/mL OVA in the presence or the absence of quercetin for 24 h. The concentrations of angiogenic factors, vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), tumor necrosis factor-α, IL-6 and IL-8 in the supernatants were examined by ELISA. BALB/c male mice immunized with OVA were challenged intranasally with OVA every other day, starting seven days after the final immunization. These mice were then orally administered quercetin once a day for five days, starting seven days after the final immunization. Clinical symptoms were assessed by counting the number of sneezes and nasal rubbing behaviors during the 10 min period just after OVA nasal provocation. The angiogenic factor concentrations in the nasal lavage fluids obtained 6 h after nasal antigenic provocation were examined by ELISA. Results: Quercetin significantly inhibited the production of angiogenetic factors induced by IgE-dependent mechanisms at 5.0 µM or more. Oral administration of 25.0 mg/kg quercetin into the mice also suppressed the appearance of angiogenetic factors in nasal lavage fluids, along with the attenuation of nasal symptoms. Conclusions: These results strongly suggest that the inhibitory action of quercetin on angiogenic factor secretion may be implicated in the therapeutic action of quercetin on allergic diseases, especially allergic rhinitis.

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Naletova, Cucci, D’Angeli, Anfuso, Magrì, La Mendola, Lupo, and Satriano. "A Tunable Nanoplatform of Nanogold Functionalised with Angiogenin Peptides for Anti-Angiogenic Therapy of Brain Tumours." Cancers 11, no. 9 (September 6, 2019): 1322. http://dx.doi.org/10.3390/cancers11091322.

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Angiogenin (ANG), an endogenous protein that plays a key role in cell growth and survival, has been scrutinised here as promising nanomedicine tool for the modulation of pro-/anti-angiogenic processes in brain cancer therapy. Specifically, peptide fragments from the putative cell membrane binding domain (residues 60–68) of the protein were used in this study to obtain peptide-functionalised spherical gold nanoparticles (AuNPs) of about 10 nm and 30 nm in optical and hydrodynamic size, respectively. Different hybrid biointerfaces were fabricated by peptide physical adsorption (Ang60–68) or chemisorption (the cysteine analogous Ang60–68Cys) at the metal nanoparticle surface, and cellular assays were performed in the comparison with ANG-functionalised AuNPs. Cellular treatments were performed both in basal and in copper-supplemented cell culture medium, to scrutinise the synergic effect of the metal, which is another known angiogenic factor. Two brain cell lines were investigated in parallel, namely tumour glioblastoma (A172) and neuron-like differentiated neuroblastoma (d-SH-SY5Y). Results on cell viability/proliferation, cytoskeleton actin, angiogenin translocation and vascular endothelial growth factor (VEGF) release pointed to the promising potentialities of the developed systems as anti-angiogenic tunable nanoplaftforms in cancer cells treatment.

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Palano, Maria Teresa, Domenica Giannandrea, Natalia Platonova, Germano Gaudenzi, Monica Falleni, Delfina Tosi, Elena Lesma, et al. "Jagged Ligands Enhance the Pro-Angiogenic Activity of Multiple Myeloma Cells." Cancers 12, no. 9 (September 11, 2020): 2600. http://dx.doi.org/10.3390/cancers12092600.

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Multiple myeloma (MM) is an incurable plasma cell malignancy arising primarily within the bone marrow (BM). During MM progression, different modifications occur in the tumor cells and BM microenvironment, including the angiogenic shift characterized by the increased capability of endothelial cells to organize a network, migrate and express angiogenic factors, including vascular endothelial growth factor (VEGF). Here, we studied the functional outcome of the dysregulation of Notch ligands, Jagged1 and Jagged2, occurring during disease progression, on the angiogenic potential of MM cells and BM stromal cells (BMSCs). Jagged1–2 expression was modulated by RNA interference or soluble peptide administration, and the effects on the MM cell lines’ ability to induce human pulmonary artery cells (HPAECs) angiogenesis or to indirectly increase the BMSC angiogenic potential was analyzed in vitro; in vivo validation was performed on a zebrafish model and MM patients’ BM biopsies. Overall, our results indicate that the MM-derived Jagged ligands (1) increase the tumor cell angiogenic potential by directly triggering Notch activation in the HPAECs or stimulating the release of angiogenic factors, i.e., VEGF; and (2) stimulate the BMSCs to promote angiogenesis through VEGF secretion. The observed pro-angiogenic effect of Notch activation in the BM during MM progression provides further evidence of the potential of a therapy targeting the Jagged ligands.

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Johnson, Benjamin, Bhagelu Achyut, Sadanand Fulzele, Ashis Mondal, Ravindra Kolhe, and Ali Arbab. "Delineating Pro-Angiogenic Myeloid Cells in Cancer Therapy." International Journal of Molecular Sciences 19, no. 9 (August 29, 2018): 2565. http://dx.doi.org/10.3390/ijms19092565.

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Recent evidence suggests that myeloid cells are critical in cancer development and therapy resistance processes. Pharmacological targeting of tumor-associated myeloid cells is an emerging approach among upcoming immune therapies. Surprisingly, myeloid cells are heterogeneous, including a subset of the myeloid cell displaying angiogenic properties in solid tumors. There is an urgent need to delineate angiogenic myeloid cell populations in order to facilitate specific targeting of protumor myeloid cells among heterogeneous pool. This review article is intended to compile all the relevant information in the literature for improved understanding of angiogenic myeloid cells and their role in tumor refractoriness to cancer therapy.

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Moroianu, J., and J. F. Riordan. "Nuclear translocation of angiogenin in proliferating endothelial cells is essential to its angiogenic activity." Proceedings of the National Academy of Sciences 91, no. 5 (March 1, 1994): 1677–81. http://dx.doi.org/10.1073/pnas.91.5.1677.

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Jin, Zhijian, Xi Cheng, Haoran Feng, Jie Kuang, Weiping Yang, Chenghong Peng, Baiyong Shen, and Weihua Qiu. "Apatinib Inhibits Angiogenesis Via Suppressing Akt/GSK3β/ANG Signaling Pathway in Anaplastic Thyroid Cancer." Cellular Physiology and Biochemistry 44, no. 4 (2017): 1471–84. http://dx.doi.org/10.1159/000485583.

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Background/Aims: Anaplastic thyroid carcinoma (ATC) is one of the most lethal human malignancies, and there is no efficient method to slow its process. Apatinib, a novel tyrosine kinase inhibitor (TKI), has been confirmed for its efficacy and safety in the treatment of advanced gastric carcinoma patients. However, the effects of Apatinib in ATC are still unknown. Methods: In this study, we explored the effects and mechanisms of Apatinib on tumor growth and angiogenesis in vitro and in vitro in ATC cells. Angiogenesis antibodies array was utilized to detect the expression of angiogenesis-related genes after Apatinib treatment in ATC cells. In addition, we used Akt activator, Akt inhibitor and GSK3β inhibitor to further study the mechanism for how Apatinib suppressed angiogenesis. Results: Apatinib treatment could suppress the growth of ATC cells in a dose- and time-dependent manner via inducing apoptosis and blocking cell cycle progression at G0/G1 phase. Moreover, Apatinib treatment decreased the expression of angiogenin (ANG) and inhibited angiogenesis of ATC cells in vitro and in vitro. We further confirmed that recombinant human ANG (rhANG) significantly abrogated Apatinib-mediated anti-angiogenic ability in ATC cells. Additionally, Apatinib treatment decreased the level of p-Akt and p-GSK3β. Moreover, the Apatinib-mediated decrease of ANG and anti-angiogenic ability were partly reversed when an Akt activator, SC79, was administered. Furthermore, the anti-angiogenic ability of Apatinib can be enhanced in the presence of Akt inhibitor, and the inhibition of GSK3β attenuated the anti-angiogenic ability of Apatinib. Conclusion: Our results demonstrated that Apatinib treatment inhibited tumor growth, and Apatinib-induced suppression of Akt/GSK3β/ANG signaling pathway may play an important role in the inhibition of angiogenesis in ATC, supporting a potential therapeutic approach for using Apatinib in the treatment of ATC.

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Ribatti, Domenico, Antonio Giovanni Solimando, and Francesco Pezzella. "The Anti-VEGF(R) Drug Discovery Legacy: Improving Attrition Rates by Breaking the Vicious Cycle of Angiogenesis in Cancer." Cancers 13, no. 14 (July 8, 2021): 3433. http://dx.doi.org/10.3390/cancers13143433.

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Resistance to anti-vascular endothelial growth factor (VEGF) molecules causes lack of response and disease recurrence. Acquired resistance develops as a result of genetic/epigenetic changes conferring to the cancer cells a drug resistant phenotype. In addition to tumor cells, tumor endothelial cells also undergo epigenetic modifications involved in resistance to anti-angiogenic therapies. The association of multiple anti-angiogenic molecules or a combination of anti-angiogenic drugs with other treatment regimens have been indicated as alternative therapeutic strategies to overcome resistance to anti-angiogenic therapies. Alternative mechanisms of tumor vasculature, including intussusceptive microvascular growth (IMG), vasculogenic mimicry, and vascular co-option, are involved in resistance to anti-angiogenic therapies. The crosstalk between angiogenesis and immune cells explains the efficacy of combining anti-angiogenic drugs with immune check-point inhibitors. Collectively, in order to increase clinical benefits and overcome resistance to anti-angiogenesis therapies, pan-omics profiling is key.

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ISHIBASHI, Hiroaki, Shingo TOKUDOME, Hideo KUROKAWA, and Minoru KAJIYAMA. "Angiogenic factors of cultured oral carcinoma cells." Japanese Journal of Oral & Maxillofacial Surgery 41, no. 5 (1995): 389–95. http://dx.doi.org/10.5794/jjoms.41.389.

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Mizrahi, Natalya, Dror Seliktar, and Eitan Kimmel. "Ultrasound-Induced Angiogenic Response in Endothelial Cells." Ultrasound in Medicine & Biology 33, no. 11 (November 2007): 1818–29. http://dx.doi.org/10.1016/j.ultrasmedbio.2007.05.007.

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García-Gómez, I., H. S. Goldsmith, J. Angulo, A. Prados, P. López-Hervás, B. Cuevas, M. Dujovny, and P. Cuevas. "Angiogenic capacity of human omental stem cells." Neurological Research 27, no. 8 (December 2005): 807–11. http://dx.doi.org/10.1179/016164105x63674.

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Hirschberg, Ruth M., Monika Sachtleben, and Johanna Plendl. "Electron microscopy of cultured angiogenic endothelial cells." Microscopy Research and Technique 67, no. 5 (2005): 248–59. http://dx.doi.org/10.1002/jemt.20204.

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Lee, S.-T., K. Chu, K.-H. Jung, H.-K. Park, D.-H. Kim, J.-J. Bahn, J.-H. Kim, et al. "Reduced circulating angiogenic cells in Alzheimer disease." Neurology 72, no. 21 (May 26, 2009): 1858–63. http://dx.doi.org/10.1212/wnl.0b013e3181a711f4.

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Brenner, S. R., J. K. Roh, S. T. Lee, K. Chu, K. H. Jung, S. K. Lee, and M. Kim. "REDUCED CIRCULATING ANGIOGENIC CELLS IN ALZHEIMER DISEASE." Neurology 74, no. 4 (January 25, 2010): 346–47. http://dx.doi.org/10.1212/wnl.0b013e3181c776d4.

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Heiss, Christian, Christian Meyer, Matthias Totzeck, Ulrike B. Hendgen-Cotta, Yvonne Heinen, Peter Luedike, Stefanie Keymel, et al. "Dietary inorganic nitrate mobilizes circulating angiogenic cells." Free Radical Biology and Medicine 52, no. 9 (May 2012): 1767–72. http://dx.doi.org/10.1016/j.freeradbiomed.2012.02.051.

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Yıldırım, Cansu, Julie Favre, Ester M. Weijers, Ruud D. Fontijn, Michiel H. van Wijhe, Sandra J. van Vliet, Reinier A. Boon, Pieter Koolwijk, Tineke C. T. M. van der Pouw Kraan, and Anton J. G. Horrevoets. "IFN-β affects the angiogenic potential of circulating angiogenic cells by activating calpain 1." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 10 (November 15, 2015): H1667—H1678. http://dx.doi.org/10.1152/ajpheart.00810.2014.

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Circulating angiogenic cells (CACs) are monocyte-derived cells with endothelial characteristics, which contribute to both angiogenesis and arteriogenesis in a paracrine way. Interferon-β (IFN-β) is known to inhibit these divergent processes in animals and patients. We hypothesized that IFN-β might act by affecting the differentiation and function of CACs. CACs were cultured from peripheral blood mononuclear cells and phenotypically characterized by surface expression of monocytic and endothelial markers. IFN-β significantly reduced the number of CACs by 18–64%. Apoptosis was not induced by IFN-β, neither in mononuclear cells during differentiation, nor after maturation to CACs. Rather, IFN-β impaired adhesion to, and spreading on, fibronectin, which was dependent on α5β1 (VLA-5)-integrin. IFN-β affected the function of VLA-5 in mature CACs, leading to rounding and detachment of cells, by induction of calpain 1 activity. Cell rounding and detachment was completely reversed by inhibition of calpain 1 activity in mature CACs. During in vitro capillary formation, CAC addition and calpain 1 inhibition enhanced sprouting of endothelial cells to a comparable extent, but were not sufficient to rescue tube formation in the presence of IFN-β. We show that the IFN-β-induced reduction of the numbers of in vitro differentiated CACs is based on activation of calpain 1, resulting in an attenuated adhesion to extracellular matrix proteins via VLA-5. In vivo, this could lead to inhibition of vessel formation due to reduction of the locally recruited CAC numbers and their paracrine angiogenic factors.

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Jun, Ji Hye, Soo Young Park, Sohae Park, Hee Jung Park, Jae Yeon Kim, Gyu Tae Park, Si Hyun Bae, Jae Ho Kim, and Gi Jin Kim. "Formyl Peptide Receptor 2 Alleviates Hepatic Fibrosis in Liver Cirrhosis by Vascular Remodeling." International Journal of Molecular Sciences 22, no. 4 (February 20, 2021): 2107. http://dx.doi.org/10.3390/ijms22042107.

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Hexapeptide WKYMVm (Trp-Lys-Tyr-Met-Val-D-Met), a ligand of formyl peptide receptor 2, exhibits anti-inflammatory and angiogenic properties in disease models. However, the therapeutic effects of WKYMVm on hepatic fibrosis have not been evaluated to date. Therefore, we investigated whether WKYMVm exerts antifibrotic effects and induces vascular regeneration in a rat model of bile duct ligation (BDL). The antifibrotic and angiogenic effects of WKYMVm on liver regeneration in the BDL rat model were analyzed using biochemical assays, qRT-PCR, western blotting, immunofluorescence, and immunohistochemistry. To determine the effects of WKYMVm on hepatic fibrosis and angiogenesis in vitro, we measured the expression levels of fibrotic factors in hepatic stellate cells (HSCs) and angiogenic factors in human umbilical vein endothelial cells (HUVECs). WKYMVm attenuated the expression of collagen type I (Col I) and α-smooth muscle actin (α-SMA) and significantly increased the levels of angiogenetic factors in the BDL model (p < 0.05). WKYMVm reduced fibrotic marker expression in transforming growth factor (TGF)-β-induced HSCs and promoted angiogenic activity through tube formation in 5-Fluorouracil (FU)-treated HUVECs (p < 0.05). Also, WKYMVm administration enhanced hepatocyte proliferation in BDL rats (p < 0.05). The WKYMVm alleviates hepatic fibrosis by inhibiting HSC activation and promotes hepatic regeneration via vascular remodeling. These data suggest that the WKYMVm may be a new therapeutic agent for liver fibrosis.

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Rae, Peter C., Richard DW Kelly, Stuart Egginton, and Justin C. St John. "Angiogenic potential of endothelial progenitor cells and embryonic stem cells." Vascular Cell 3, no. 1 (2011): 11. http://dx.doi.org/10.1186/2045-824x-3-11.

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Lardon, Jessy, Ilse Rooman, and Luc Bouwens. "Nestin expression in pancreatic stellate cells and angiogenic endothelial cells." Histochemistry and Cell Biology 117, no. 6 (May 14, 2002): 535–40. http://dx.doi.org/10.1007/s00418-002-0412-4.

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Ronca, Roberto, Sara Taranto, Michela Corsini, Chiara Tobia, Cosetta Ravelli, Sara Rezzola, Mirella Belleri, et al. "Pentraxin 3 Inhibits the Angiogenic Potential of Multiple Myeloma Cells." Cancers 13, no. 9 (May 8, 2021): 2255. http://dx.doi.org/10.3390/cancers13092255.

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During multiple myeloma (MM) progression the activation of the angiogenic process represents a key step for the formation of the vascular niche, where different stromal components and neoplastic cells collaborate and foster tumor growth. Among the different pro-angiogenic players, Fibroblast Growth Factor 2 (FGF2) plays a pivotal role in BM vascularization occurring during MM progression. Long Pentraxin 3 (PTX3), a natural FGF antagonist, is able to reduce the activation of stromal components promoted by FGF2 in various in vitro models. An increased FGF/PTX3 ratio has also been found to occur during MM evolution, suggesting that restoring the “physiological” FGF/PTX3 ratio in plasma cells and BM stromal cells (BMSCs) might impact MM. In this work, taking advantage of PTX3-inducible human MM models, we show that PTX3 produced by tumor cells is able to restore a balanced FGF/PTX3 ratio sufficient to prevent the activation of the FGF/FGFR system in endothelial cells and to reduce the angiogenic capacity of MM cells in different in vivo models. As a result of this anti-angiogenic activity, PTX3 overexpression causes a significant reduction of the tumor burden in both subcutaneously grafted and systemic MM models. These data pave the way for the exploitation of PTX3-derived anti-angiogenic approaches in MM.

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Stewart, E., R. Wei, M. Uribe, S. May, and W. Amoaku. "Stimulation of TLR4 Increases Angiogenic and Anti-Angiogenic Gene Expression in Choroidal Endothelial Cells." Acta Ophthalmologica 93 (September 23, 2015): n/a. http://dx.doi.org/10.1111/j.1755-3768.2015.0627.

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Koparal, Ayşe Tansu. "Anti-angiogenic and antiproliferative properties of the lichen substances (-)-usnic acid and vulpinic acid." Zeitschrift für Naturforschung C 70, no. 5-6 (May 1, 2015): 159–64. http://dx.doi.org/10.1515/znc-2014-4178.

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Abstract The anti-proliferative activities of the lichen substances (-)-usnic acid and vulpinic acid on the viability of HepG2 hepatocarcinoma cells, NS20Y neuroblastoma cells and HUVEC endothelial cells were studied by the MTT assay. The anti-angiogenic potential of the substances was determined by the endothelial tube formation assay. Both lichen substances exhibited strong anti-angiogenic activity and were more cytotoxic to the cancer cell lines than to the normal cell line, but vulpinic acid has more potential as an anti-angiogenic substance because of its low cytotoxicity and stronger anti-angiogenic activity on the HUVEC cell line.

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Ueda, Eric, Ugur Ozerdem, Yen-Hao Chen, Min Yao, Kuang Tzu Huang, Huiqin Sun, Manuela Martins-Green, Paolo Bartolini, and Ameae M. Walker. "A molecular mimic demonstrates that phosphorylated human prolactin is a potent anti-angiogenic hormone." Endocrine-Related Cancer 13, no. 1 (March 2006): 95–111. http://dx.doi.org/10.1677/erc.1.01076.

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S179D prolactin (PRL) is an experimentally useful mimic of naturally phosphorylated human prolactin. S179D PRL, but not unmodified PRL, was found to be anti-angiogenic in both the chorioallantoic membrane and corneal assays. Further investigation using human endothelial in vitro models showed reduced cell number, reduced tubule formation in Matrigel, and reduced migration and invasion, as a function of treatment with S179D PRL. Analysis of growth factors in human endothelial cells in response to S179D PRL showed: a decreased expression or release of endogenous PRL, heme-oxygenase-1, basic fibroblast growth factor (bFGF), angiogenin, epidermal growth factor and vascular endothelial growth factor; and an increased expression of inhibitors of matrix metalloproteases. S179D PRL also blocked signaling from bFGF in these cells. We conclude that this molecular mimic of a pituitary hormone is a potent anti-angiogenic protein, partly as a result of its ability to reduce utilization of several well-established endothelial autocrine growth loops, partly by its ability to block signaling from bFGF and partly because of its ability to decrease endothelial migration. These findings suggest that circulating levels of phosphorylated PRL may influence the progression of cancer and, furthermore, that S179D PRL may be a useful anti-angiogenic therapeutic.

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Sun, Cheng, Shi-Bin Feng, Zheng-Wang Cao, Jun-Jie Bei, Qiang Chen, Xian-Jie Xu, Zhou Zhou, Zheng-Ping Yu, and Hou-Yuan Hu. "Up-Regulated Expression of Matrix Metalloproteinases in Endothelial Cells Mediates Platelet Microvesicle-Induced Angiogenesis." Cellular Physiology and Biochemistry 41, no. 6 (2017): 2319–32. http://dx.doi.org/10.1159/000475651.

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Background/Aims: Platelet microvesicles (PMVs) contribute to angiogenesis and vasculogenesis, but the mechanisms underlying these contributions have not been fully elucidated. In the present study, we investigated whether PMVs regulate the angiogenic properties of endothelial cells (ECs) via mechanisms extending beyond the transport of angiogenic regulators from platelets. Methods: In vitro Matrigel tube formation assay and in vivo Matrigel plug assay were used to evaluate the pro-angiogenic activity of PMVs. The effects of PMVs on the migration of human umbilical vein endothelial cells (HUVECs) were detected by transwell assay and wound-healing assay. Real-time PCR and western blot were conducted to examine mRNA and protein expression of pro-angiogenic factors in HUVECs. Matrix metalloproteinase (MMP) activity was assayed by gelatin zymography. Moreover, the effects of specific MMP inhibitors were tested. Results: PMVs promoted HUVEC capillary-like network formation in a dose-dependent manner. Meanwhile, PMVs dose-dependently facilitated HUVEC migration. Levels of MMP-2 and MMP-9 expression and activity were up-regulated in HUVECs stimulated with PMVs. Inhibition of MMPs decreased their pro-angiogenic and pro-migratory effects on HUVECs. Moreover, we confirmed the pro-angiogenic activity of PMVs in vivo in mice with subcutaneous implantation of Matrigel, and demonstrated that blockade of MMPs attenuated PMV-induced angiogenesis. Conclusion: The findings of our study indicate that PMVs promote angiogenesis by up-regulating MMP expression in ECs via mechanism extending beyond the direct delivery of angiogenic factors.

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Okamoto, Takayuki, Haruki Usuda, Tetsuya Tanaka, Koichiro Wada, and Motomu Shimaoka. "The Functional Implications of Endothelial Gap Junctions and Cellular Mechanics in Vascular Angiogenesis." Cancers 11, no. 2 (February 18, 2019): 237. http://dx.doi.org/10.3390/cancers11020237.

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Angiogenesis—the sprouting and growth of new blood vessels from the existing vasculature—is an important contributor to tumor development, since it facilitates the supply of oxygen and nutrients to cancer cells. Endothelial cells are critically affected during the angiogenic process as their proliferation, motility, and morphology are modulated by pro-angiogenic and environmental factors associated with tumor tissues and cancer cells. Recent in vivo and in vitro studies have revealed that the gap junctions of endothelial cells also participate in the promotion of angiogenesis. Pro-angiogenic factors modulate gap junction function and connexin expression in endothelial cells, whereas endothelial connexins are involved in angiogenic tube formation and in the cell migration of endothelial cells. Several mechanisms, including gap junction function-dependent or -independent pathways, have been proposed. In particular, connexins might have the potential to regulate cell mechanics such as cell morphology, cell migration, and cellular stiffness that are dynamically changed during the angiogenic processes. Here, we review the implication for endothelial gap junctions and cellular mechanics in vascular angiogenesis.

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Fens, Marcel H. A. M., Enrico Mastrobattista, Anko M. de Graaff, Frits M. Flesch, Anton Ultee, Jan T. Rasmussen, Grietje Molema, Gert Storm, and Raymond M. Schiffelers. "Angiogenic endothelium shows lactadherin-dependent phagocytosis of aged erythrocytes and apoptotic cells." Blood 111, no. 9 (May 1, 2008): 4542–50. http://dx.doi.org/10.1182/blood-2007-06-094763.

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Abstract Angiogenic endothelium plays a crucial role in tumor growth. During angiogenesis, complex alterations in the microenvironment occur. In response, the endothelium undergoes phenotypic changes, for example overexpression of αv-integrins. Here, we show that the overexpression of αv-integrins on angiogenic endothelial cells is engaged in phagocytic actions involving binding (“tethering”) and uptake (“tickling”) of lactadherin (also termed MFG-E8)–opsonized particles. Phosphatidylserine (PS)–exposing multilamellar vesicles, “aged” erythrocytes, and apoptotic melanoma cells incubated with lactadherin were all phagocytosed by angiogenic endothelial cells in vitro. Furthermore, we demonstrated lactadherin expression in and around tumor blood vessels making opsonization in situ plausible. By engineering the surface of erythrocytes with covalently coupled cyclic Arg-Gly-Asp (RGD) peptides—mimicking lactadherin opsonization—we could induce phagocytosis by angiogenic endothelial cells both in vitro and in vivo. In vitro, this was confirmed by cytochalasin D preincubation. When RGD-erythrocytes were administered intravenously in tumor-bearing mice, blood vessel congestion followed by tumor core necrosis was seen. Moreover, RGD-erythrocytes could delay tumor growth in a murine melanoma model, possibly through induction of tumor infarctions. These results reveal that angiogenic endothelial cells have phagocytic properties for lactadherin-opsonized large particles and apoptotic cells. Implications of our findings for diagnostic and therapy of angiogenesis-driven diseases are discussed.

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Rohde, Eva, Katharina Schallmoser, Andreas Reinisch, Nicole A. Hofmann, Thomas Pfeifer, Gerald Rechberger, Dagmar Kratky, Eleonore Fröhlich, and Dirk Strunk. "Pro–angiogenic Induction of Myeloid Cells for Therapeutic Angiogenesis Can Favor MAPK p38–dependent Foam Cell Formation." Blood 116, no. 21 (November 19, 2010): 4442. http://dx.doi.org/10.1182/blood.v116.21.4442.4442.

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Abstract Abstract 4442 Background: Clinical trials for therapeutic angiogenesis use blood- or marrow-derived transplants containing hematopoietic cells, endothelial progenitor cells (EPCs) and mesenchymal stem and progenitor cells (MSPCs) to support vascular regeneration. Recently concerns have emerged, as bone marrow-derived stem cell preparations also include these three cell types which probably may contribute to atherosclerosis. We therefore asked whether human myelomonocytic hematopoietic cells, EPCs or MSPCs after pro-angiogenic induction can accumulate lipid droplets (LDs) and develop into foam cells. Method: LD accumulation was quantified by flow cytometry, confocal microscopy and cholesterol measurement in each of the tested cell types. The impact of an initial three-day pro-angiogenic culture on subsequent foam cell formation was studied to mimic a relevant setting already being used in clinical trials. The phosphorylation state of intracellular signaling molecules in response to pro-angiogenic stimulation was determined to delineate the operative mechanisms and to establish a basis for interventional strategies. Result: Foam cells were formed by monocytes but neither by EPCs nor by MSPCs after pro-angiogenic induction. Mitogen-activated protein kinase (MAPK) p38 phosphorylation was enhanced in monocytes after pro-angiogenic stimulation. Kinase inhibition almost abrogated intracellular LD accumulation. Conclusion: These data suggest that hematopoietic cell preparations containing monocytes bear the risk of foam cell formation after pro-angiogenic induction. EPCs and MSPCs instead may drive vascular regeneration without atherogenesis aggravation. A thorough understanding of cell biology is necessary to develop new strategies combining pro-angiogenic and anti-atherogenic cellular effects during therapeutic angiogenesis. Disclosures: No relevant conflicts of interest to declare.

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Kanayasu-Toyoda, Toshie, Takeshi Tanaka, Akiko Ishii-Watabe, Hiroko Kitagawa, Akifumi Matsuyama, Eriko Uchida, and Teruhide Yamaguchi. "Angiogenic Role of MMP-2/9 Expressed on the Cell Surface of Early Endothelial Progenitor Cells/Myeloid Angiogenic Cells." Journal of Cellular Physiology 230, no. 11 (July 27, 2015): 2763–75. http://dx.doi.org/10.1002/jcp.25002.

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He, Ting, Feifei Qi, Lin Jia, Shan Wang, Chunying Wang, Nan Song, Yan Fu, Lin Li, and Yongzhang Luo. "Tumor cell-secreted angiogenin induces angiogenic activity of endothelial cells by suppressing miR-542-3p." Cancer Letters 368, no. 1 (November 2015): 115–25. http://dx.doi.org/10.1016/j.canlet.2015.07.036.

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Ribatti, Domenico, Marco Presta, Angelo Vacca, Roberto Ria, Roberta Giuliani, Patrizia Dell’Era, Beatrice Nico, Luisa Roncali, and Franco Dammacco. "Human Erythropoietin Induces a Pro-Angiogenic Phenotype in Cultured Endothelial Cells and Stimulates Neovascularization In Vivo." Blood 93, no. 8 (April 15, 1999): 2627–36. http://dx.doi.org/10.1182/blood.v93.8.2627.

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Abstract Hematopoietic and endothelial cell lineages share common progenitors. Accordingly, cytokines formerly thought to be specific for the hematopoietic system have been shown to affect several functions in endothelial cells, including angiogenesis. In this study, we investigated the angiogenic potential of erythropoietin (Epo), the main hormone regulating proliferation, differentiation, and survival of erythroid cells. Epo receptors (EpoRs) have been identified in the human EA.hy926 endothelial cell line by Western blot analysis. Also, recombinant human Epo (rHuEpo) stimulates Janus Kinase-2 (JAK-2) phosphorylation, cell proliferation, and matrix metalloproteinase-2 (MMP-2) production in EA.hy926 cells and significantly enhances their differentiation into vascular structures when seeded on Matrigel. In vivo, rHuEpo induces a potent angiogenic response in the chick embryo chorioallantoic membrane (CAM). Accordingly, endothelial cells of the CAM vasculature express EpoRs, as shown by immunostaining with an anti-EpoR antibody. The angiogenic response of CAM blood vessels to rHuEpo was comparable to that elicited by the prototypic angiogenic cytokine basic fibroblast growth factor (FGF2), it occurred in the absence of a significant mononuclear cell infiltrate, and it was not mimicked by endothelin-1 (ET-1) treatment. Taken together, these data demonstrate the ability of Epo to interact directly with endothelial cells and to elicit an angiogenic response in vitro and in vivo and thus act as a bona fide direct angiogenic factor.

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Ribatti, Domenico, Marco Presta, Angelo Vacca, Roberto Ria, Roberta Giuliani, Patrizia Dell’Era, Beatrice Nico, Luisa Roncali, and Franco Dammacco. "Human Erythropoietin Induces a Pro-Angiogenic Phenotype in Cultured Endothelial Cells and Stimulates Neovascularization In Vivo." Blood 93, no. 8 (April 15, 1999): 2627–36. http://dx.doi.org/10.1182/blood.v93.8.2627.408k21_2627_2636.

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Hematopoietic and endothelial cell lineages share common progenitors. Accordingly, cytokines formerly thought to be specific for the hematopoietic system have been shown to affect several functions in endothelial cells, including angiogenesis. In this study, we investigated the angiogenic potential of erythropoietin (Epo), the main hormone regulating proliferation, differentiation, and survival of erythroid cells. Epo receptors (EpoRs) have been identified in the human EA.hy926 endothelial cell line by Western blot analysis. Also, recombinant human Epo (rHuEpo) stimulates Janus Kinase-2 (JAK-2) phosphorylation, cell proliferation, and matrix metalloproteinase-2 (MMP-2) production in EA.hy926 cells and significantly enhances their differentiation into vascular structures when seeded on Matrigel. In vivo, rHuEpo induces a potent angiogenic response in the chick embryo chorioallantoic membrane (CAM). Accordingly, endothelial cells of the CAM vasculature express EpoRs, as shown by immunostaining with an anti-EpoR antibody. The angiogenic response of CAM blood vessels to rHuEpo was comparable to that elicited by the prototypic angiogenic cytokine basic fibroblast growth factor (FGF2), it occurred in the absence of a significant mononuclear cell infiltrate, and it was not mimicked by endothelin-1 (ET-1) treatment. Taken together, these data demonstrate the ability of Epo to interact directly with endothelial cells and to elicit an angiogenic response in vitro and in vivo and thus act as a bona fide direct angiogenic factor.

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Asosingh, Kewal, Hendrik De Raeve, Eline Menu, Ivan Van Riet, Eric Van Marck, Benjamin Van Camp, and Karin Vanderkerken. "Angiogenic switch during 5T2MM murine myeloma tumorigenesis: role of CD45 heterogeneity." Blood 103, no. 8 (April 15, 2004): 3131–37. http://dx.doi.org/10.1182/blood-2003-08-2946.

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Abstract The active role of angiogenesis during disease progression is well recognized in solid tumors. In hematologic malignancies such as multiple myeloma (MM), it is not known whether tumor neovascularization is an epiphenomenon or whether it is actively involved in disease progression. At clinical presentation, myeloma disease and the associated angiogenesis are both well established. Here the 5T2MM murine model was used to analyze angiogenesis during preclinical myeloma stages. Bone marrow (BM) of 5T2MM-inoculated mice was analyzed at weekly intervals until the end stage of the disease. Histologic analysis and assessment of microvessel density (MVD) by CD31 staining demonstrated a preangiogenic stage of small tumor aggregates followed by an angiogenic switch and subsequently an angiogenic stage of progressive tumor growth and large, confluent tumor nodules. Flow cytometric analysis that indicated an increase in percentage CD45- MM cells preceded the angiogenic switch. Real-time polymerase chain reaction (RT-PCR) of sorted CD45+ and CD45- MM cells indicated higher vascular endothelial growth factor 120 (VEGF120) and VEGF164 transcripts in CD45- MM cells. VEGF enzyme-linked immunosorbent assay (ELISA) revealed high secretion by CD45- MM cells but no protein secretion by CD45+ MM cells, indicating angiogenic heterogeneity among the MM cells. These data suggest that, like in solid tumors, angiogenic switch and angiogenic heterogeneity exist in MM. (Blood. 2004;103:3131-3137)

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Capoccia, Ben J., Rebecca M. Shepherd, and Daniel C. Link. "G-CSF and AMD3100 Mobilize Angiogenic Cells into the Blood That Stimulate Angiogenesis In Vivo through a Paracrine Mechanism." Blood 106, no. 11 (November 16, 2005): 188. http://dx.doi.org/10.1182/blood.v106.11.188.188.

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Abstract There is compelling evidence that circulating angiogenic cells exist in humans that are able to home to sites of vascular injury and stimulate angiogenesis. However, under normal conditions, the number of these cells in the blood is small, potentially limiting the angiogenic response. Certain cytokines, including G-CSF, are able to mobilize angiogenic cells into the blood, potentially circumventing this limitation. Previously, we reported that treatment with G-CSF and AMD3100, a novel CXCR4 antagonist, significantly improved revascularization in a mouse model of acute hindlimb ischemia. Interestingly, the kinetics of angiogenic cell mobilization were distinct, with maximal improvement in blood flow observed on days 5–7 in the AMD3100 treated cohort versus 10–14 in the G-CSF treated cohort. Accordingly, combination treatment with G-CSF and AMD3100 resulted in the earliest and most robust angiogenic response. This regimen may merit investigation in future clinical trials of circulating angiogenic cells for the treatment of ischemic vascular diseases. In the present study, the mechanism by which these agents stimulate angiogenesis was explored. We first performed adoptive transfer studies. Blood mononuclear cells from G-CSF and AMD3100 treated mice were infused intravenously into recipient mice 24 hours after the induction of hindlimb ischemia. Perfusion in the ischemic hindlimb was significantly improved in mice receiving adoptively transferred cells compared to saline treated controls (overall effect of treatment, p<0.0001). Moreover, capillary density in the ischemic hindlimb was significantly increased in mice that had received adoptively transferred cells (p=0.0004). Interestingly, on a per cell basis, blood mononuclear cells from un-mobilized mice were equally effective as G-CSF and AMD3100 mobilized blood mononuclear cells in inducing revascularization. Together, these observations suggest that these agents improve angiogenesis by increasing the basal number of circulating angiogenic cells rather than mobilizing a unique angiogenic cell population. The ability of circulating angiogenic cells to directly incorporate into neoendothelium is controversial. To address this issue, blood mononuclear cells from Tie2GFP transgenic mice were adoptively transferred into non-transgenic FVB mice following the induction of hindlimb ischemia. Importantly, GFP expression in Tie2GFP transgenic mice is mainly limited to endothelial cells. Thus, if adoptively transferred cells directly contribute to the neovasculature, GFP+ endothelial cells should be apparent in recipient mice. Endothelial cell chimerism in the adductor muscle from the ischemic limb was analyzed 2 weeks post surgery using a novel flow cytometry-based assay. Essentially no GFP+ cells were detected, showing that the great majority of neoendothelium was of recipient origin. These data were confirmed by histological assays showing that von Willibrand factor-positive endothelial cells in the ischemic muscle of these mice did not co-express GFP. Collectively, these data show that treatment with G-CSF or AMD3100 potently stimulates angiogenesis at sites of ischemia by mobilizing angiogenic cells into the blood. These cells are able to home to sites of injury where they stimulate angiogenesis in a paracrine fashion.

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Sheela, S., V. M. Riccardi, and N. Ratner. "Angiogenic and invasive properties of neurofibroma Schwann cells." Journal of Cell Biology 111, no. 2 (August 1, 1990): 645–53. http://dx.doi.org/10.1083/jcb.111.2.645.

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Neurofibromas are benign tumors from patients with von Recklinghausen Neurofibromatosis (NF1) that are comprised primarily of Schwann cells. These Schwann cells are found both in association with axons and in the extracellular matrix that is prevalent in neurofibromas, and in which fibroblasts are also abundant. An unresolved question has been whether cells in neurofibromas are normal cells or are intrinsically abnormal. We have tested the hypothesis that cells in neurofibromas are abnormal and have shown that neurofibroma Schwann cells, unlike normal Schwann cells, promote angiogenesis in the chick chorioallantoic membrane model system, and invade basement membranes in this system. In contrast, neurofibroma fibroblasts neither promote angiogenic reactions nor invade basement membranes. When injected into nude mice, neurofibroma Schwann cells do not form progressive tumors. These results suggest that NF1 Schwann cells differ from normal Schwann cells, that they are preneoplastic, and that genetic and/or epigenetic changes in Schwann cells may be required for development of peripheral nerve tumors in NF1.

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Nogueras, Sonia, Ana Merino, Raquel Ojeda, Julia Carracedo, Mariano Rodriguez, Alejandro Martin-Malo, Rafael Ramírez, and Pedro Aljama. "Coupling of endothelial injury and repair: an analysis using an in vivo experimental model." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 2 (February 2008): H708—H713. http://dx.doi.org/10.1152/ajpheart.00466.2007.

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The repair of the endothelium after inflammatory injury is essential to maintaining homeostasis. The link between inflammation-induced endothelial damage and repair has not been fully characterized in vivo. We have developed a rat model to evaluate the coupling of lipopolysaccharide (LPS)-induced endothelial injury and repair. Aortic endothelium injury was analyzed by both inmunohistochemistry and flow cytometry to quantify the number of endothelial cells and the percentage of apoptotic endothelial cells. We have also identified the percentage of circulating angiogenic cells capable of repairing the damaged endothelium. Erythropoietin was administered to inhibit LPS-induced endothelial apoptosis. Loss of the normal endothelial structure was observed in the aorta of the animals treated with LPS. Eight hours after LPS administration, the number of endothelial cells decreased by 40%, returning to normal after 24 h. There was a threefold increase in the percentage of circulating angiogenic cells, which did not return to normal levels until 48 h after LPS administration. Circulating angiogenic cell levels did not change when LPS-induced endothelial damage was prevented by erythropoietin. The endothelial injury caused by inflammation activates the mobilization of circulating angiogenic cells, thus completing endothelial repair. Inflammation without endothelial injury does not trigger the mobilization of circulating angiogenic cells.

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Ciciola, Paola, Priscilla Cascetta, Cataldo Bianco, Luigi Formisano, and Roberto Bianco. "Combining Immune Checkpoint Inhibitors with Anti-Angiogenic Agents." Journal of Clinical Medicine 9, no. 3 (March 3, 2020): 675. http://dx.doi.org/10.3390/jcm9030675.

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Immunotherapy has recently emerged as a novel strategy for treating different types of solid tumors, with promising results. However, still a large fraction of patients do not primarily respond to such approaches, and even responders sooner or later develop resistance. Moreover, immunotherapy is a promising strategy for certain malignancies but not for others, with this discrepancy having been attributed to a more immunogenic microenvironment of some tumors. As abnormal and augmented tumor vessels often occur in cancerogenesis, anti-angiogenic drugs have already demonstrated their effectiveness both in preclinical and in clinical settings. By targeting abnormal formation of tumor vessels, anti-angiogenetic agents potentially result in an enhanced infiltration of immune effector cells. Moreover, crosstalks downstream of the immune checkpoint axis and vascular endothelial growth factor receptor (VEGFR) signaling may result in synergistic effects of combined treatment in tumor cells. In this review, we will describe and discuss the biological rationale of a combined therapy, underlying the modification in tumor microenvironment as well as in tumor cells after exposure to checkpoint inhibitors and anti-angiogenic drugs. Moreover, we will highlight this strategy as a possible way for overcoming drug resistance. By first discussing potential prognostic and predictive factors for combined treatment, we will then turn to clinical settings, focusing on clinical trials where this strategy is currently being investigated.

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Ross, Mark D., Eva M. Malone, Richard Simpson, Islay Cranston, Lesley Ingram, Graham P. Wright, George Chambers, and Geraint Florida-James. "Lower resting and exercise-induced circulating angiogenic progenitors and angiogenic T cells in older men." American Journal of Physiology-Heart and Circulatory Physiology 314, no. 3 (March 2018): H392—H402. http://dx.doi.org/10.1152/ajpheart.00592.2017.

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McNeill, B., B. Vulesevic, M. Ruel, and E. J. Suuronen. "Integrin α5 Mediates the Pro-Angiogenic Potency of Circulating Angiogenic Cells Cultured on Collagen Matrices." Canadian Journal of Cardiology 29, no. 10 (October 2013): S384. http://dx.doi.org/10.1016/j.cjca.2013.07.660.

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Lee, Jung, Daniel Balikov, Jae Yang, Ki Kim, Hun Park, Jeong Kim, Il Kwon, Leon Bellan, and Hak-Joon Sung. "Cationic Nanocylinders Promote Angiogenic Activities of Endothelial Cells." Polymers 8, no. 1 (January 14, 2016): 15. http://dx.doi.org/10.3390/polym8010015.

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Journal articles on the topic 'Angiogenic cells'

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