Relevant bibliographies by topics / Matrigel plug assay

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Academic literature on the topic 'Matrigel plug assay'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Matrigel plug assay"

1

Aref, Zeen, and Paul H. A. Quax. "In Vivo Matrigel Plug Assay as a Potent Method to Investigate Specific Individual Contribution of Angiogenesis to Blood Flow Recovery in Mice." International Journal of Molecular Sciences 22, no. 16 (August 18, 2021): 8909. http://dx.doi.org/10.3390/ijms22168909.

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Neovascularization restores blood flow recovery after ischemia in peripheral arterial disease. The main two components of neovascularization are angiogenesis and arteriogenesis. Both of these processes contribute to functional improvements of blood flow after occlusion. However, discriminating between the specific contribution of each process is difficult. A frequently used model for investigating neovascularization is the murine hind limb ischemia model (HLI). With this model, it is difficult to determine the role of angiogenesis, because usually the timing for the sacrifice of the mice is chosen to be optimal for the analysis of arteriogenesis. More importantly, the occurring angiogenesis in the distal calf muscles is probably affected by the proximally occurring arteriogenesis. Therefore, to understand and subsequently intervene in the process of angiogenesis, a model is needed which investigates angiogenesis without the influence of arteriogenesis. In this study we evaluated the in vivo Matrigel plug assay in genetic deficient mice to investigate angiogenesis. Mice deficient for interferon regulatory factor (IRF)3, IRF7, RadioProtective 105 (RP105), Chemokine CC receptor CCR7, and p300/CBP-associated factor (PCAF) underwent the in vivo Matrigel model. Histological analysis of the Matrigel plugs showed an increased angiogenesis in mice deficient of IRF3, IRF7, and RP105, and a decreased angiogenesis in PCAF deficient mice. Our results also suggest an involvement of CCR7 in angiogenesis. Comparing our results with results of the HLI model found in the literature suggests that the in vivo Matrigel plug assay is superior in evaluating the angiogenic response after ischemia.
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2

Meng, Shu, Jie Lv, Palas K. Chanda, Iris Owusu, Kaifu Chen, and John P. Cooke. "Reservoir of Fibroblasts Promotes Recovery From Limb Ischemia." Circulation 142, no. 17 (October 27, 2020): 1647–62. http://dx.doi.org/10.1161/circulationaha.120.046872.

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Background: The angiogenic response to ischemia restores perfusion so as to preserve tissue. A role for mesenchymal-to-endothelial transition in the angiogenic response is controversial. This study is to determine if resident fibroblasts contribute to angiogenesis. Methods: We utilized the murine model of hindlimb ischemia, and in vivo Matrigel plug assay together with lineage tracing studies and single cell RNA-sequencing to examine the transcriptional and functional changes in fibroblasts in response to ischemia. Results: Lineage tracing using Fsp1-Cre: R26R-EYFP mice revealed the emergence within the ischemic hindlimb of a small subset of YFP + CD144 + CD11b − fibroblasts (E* cells) that expressed endothelial cell (EC) genes. Subcutaneous administration of Matrigel in Fsp1-Cre: R26R-EYFP mice generated a plug that became vascularized within 5 days. Isolation of YFP + CD11b - cells from the plug revealed a small subset of YFP + CD144 + CD11b − E* cells which expressed EC genes. Pharmacological or genetic suppression of innate immune signaling reduced vascularity of the Matrigel plug and abrogated the generation of these E* cells. These studies were repeated using human fibroblasts, with fluorescence-activated cell sorting analysis revealing that a small percentage of human fibroblasts that were induced to express EC markers in Matrigel plug assay. Pharmacological suppression or genetic knockout of inflammatory signaling abolished the generation of E* cells, impaired perfusion recovery and increased tissue injury after femoral artery ligation. To further characterize these E* cells, single cell RNA-sequencing studies were performed and revealed 8 discrete clusters of cells expressing characteristic fibroblast genes, of which 2 clusters (C5 and C8) also expressed some EC genes. Ischemia of the hindlimb induced expansion of clusters C5 and C8. The C8 cells did not express CD144, nor did they form networks in Matrigel, but did generate angiogenic cytokines. The C5 fibroblasts most resembled E* cells in their expression of CD144 and their ability to form EC-like networks in Matrigel. Conclusions: Together, these studies indicate the presence of subsets of tissue fibroblasts which seem poised to contribute to the angiogenic response. The expansion of these subsets with ischemia is dependent on activation of innate immune signaling and contributes to recovery of perfusion and preservation of ischemic tissue.
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3

Kwon, Oh Sung, Myoung Seok Jeong, Bonglee Kim, and Sung-Hoon Kim. "Antiangiogenic Effect of Ethanol Extract ofVigna angularisvia Inhibition of Phosphorylation of VEGFR2, Erk, and Akt." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/371368.

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Though dietary azuki bean (Vigna angularis) seed containing antioxidant proanthocyanidins was known to have multibiological activities including antioxidant, hypotensive, anti-inflammatory, and immunomodulatory activities, the antiangiogenic activity of ethanol extract ofVigna angularis(EVA) was never reported so far. In the present study, the antiangiogenic mechanism of EVA was examined in human umbilical vein endothelial cells (HUVECs). EVA showed weak cytotoxicity in HUVECs, while it significantly suppressed the VEGF induced proliferation of HUVECs. Consistently, wound healing assay revealed that EVA inhibited the VEGF induced migration of HUVECs. Also, EVA abrogated the VEGF induced tube formation of HUVECs in a concentration dependent fashion. Furthermore, Matrigel plug assay showed that EVA significantly reduced the hemoglobin level of Matrigel plug in mice compared to untreated control. Of note, EVA effectively attenuated the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs. Overall, our findings suggest that EVA inhibits angiogenesis in VEGF-treated HUVECs via inhibition of phosphorylation of VEGFR2, ERK, and Akt.
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Coltrini, Daniela, Emanuela Di Salle, Roberto Ronca, Mirella Belleri, Chiara Testini, and Marco Presta. "Matrigel plug assay: evaluation of the angiogenic response by reverse transcription-quantitative PCR." Angiogenesis 16, no. 2 (November 11, 2012): 469–77. http://dx.doi.org/10.1007/s10456-012-9324-7.

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5

Lopes, Fláavia Cristine Mascia, Raquel Costa, Sara T. Olalla Saad, Raquel Soares, Fernando Ferreira Costa, and Nicola Conran. "Proangiogenic Effects of Plasma From Sickle Cell Disease Patients and Antiangiogenic Effects of Hydroxyurea: Evaluation of Invasion and Proliferation of Human Endothelial Cells and Effects of Hydroxyurea in a Mouse Matrigel Plug Neovascularization Assay." Blood 120, no. 21 (November 16, 2012): 377. http://dx.doi.org/10.1182/blood.v120.21.377.377.

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Abstract Abstract 377 Sickle Cell Disease (SCD) results from mutations in the β hemoglobin chain and is associated with a complex pathophysiology that often involves recurrent vasoocclusion in association with vascular inflammation, oxidative stress, ischemia-reperfusion injury and endothelial activation. Dysregulation of angiogenesis occurs in various pathologies and a newly recognized proangiogenic state is associated with SCD. Central to the process of angiogenesis are the endothelial cells (EC) that are activated by angiogenic signals and release degrading enzymes that allow EC to migrate, proliferate and finally differentiate to form new vessels. In keeping with this proposed proangiogenic state, we previously found that plasma from SCD patients increases human umbilical vein endothelial cell (HUVEC) tube formation on Matrigel. In contrast, plasma from SCD patients treated with hydroxyurea (HU; a drug that has been used successfully for SCD therapy) inhibited the ability of HUVEC to form branching and thick anastomosing capillaries in the same model. In the present study, we aimed to determine the effects of plasma from SCD patients on additional HUVEC functions associated with key steps of angiogenesis, including invasion and proliferation, as well as further evaluating the direct antiangiogenic effects of HU with a mouse Matrigel plug neovascularization assay. Steady-state HbSS (SS), steady-state HbSS treated with HU (SSHU, 20–30mg/kg/day HU) and healthy control individuals (CON) were recruited for the study. Invasive cell behavior in the presence of 10 % plasma was quantified in vitro using a double-chamber assay. Under the same conditions, cell proliferation analyses were carried out using cellular incorporation of bromodeoxyuridine. Interestingly, an effective increase of 39.66 ± 29.54% in EC invasion was observed in the presence of SS plasma (P<0.05, N=5) compared to basal cell invasion. In contrast, SSHU plasma resulted in a significant decrease in cell invasive ability (51.94 ± 7.82% reduction; N=5, P<0.001). Accordingly, when the proliferative activity of SS plasma was investigated, increased cell proliferation was observed (13.73 ± 3.41%, compared to basal EC proliferation; N=5, P<0.05). Plasma from SSHU individuals significantly reduced HUVEC proliferation by 24.90 ± 3.45% (P<0.0, N=5). In contrast, CON plasma did not modify either the invasive or proliferative activities of HUVECs. For the Matrigel plug assay, C57BL/6 mice received subcutaneous Matrigel plugs supplemented, or not, with 100μM HU in the presence or absence of vascular endothelial growth factor (VEGF). After seven days, the plugs were removed and Matrigel hemoglobin content measured, using Drabkin's method. The positive control group (VEGF) presented extensive neovascularization of the Matrigel, as shown by the red color distributed in the whole plug. In contrast, Matrigel implants treated with both VEGF and HU demonstrated a strong inhibition of vascular development (67.53 ± 6.68% reduction in neovascularization; N=6, P<0.05) that was similar to that of negative controls (Matrigel not treated with VEGF). Data presented herein show that important features of the angiogenic process, endothelial cell invasion and proliferation, can be upregulated by plasma from SCD patients, confirming the apparent proangiogenic status of these individuals. In contrast, plasma from patients treated with HU exerted antiangiogenic effects by inhibiting the same angiogenic steps. Furthermore, HU was found to have direct antiangiogenic effects in in vivo assays. To our knowledge, this is the first report of the antiangiogenic activity of HU in a mouse model. Balancing angiogenesis is essential for SCD individuals, as enhanced angiogenesis may increase the incidence of manifestations such as proliferative retinopathy and pulmonary hypertension. On the other hand, angiogenesis is essential for mechanisms such as ulcer recovery, neovascularization of ischemic tissues and tissue regeneration and it may be that HU therapy may retard such processes. In conclusion, this study finds further evidence for a proangiogenic state in SCD. HU inhibits key steps in angiogenic mechanisms, demonstrating a possible use for this drug in the treatment of pathological angiogenesis in this and other diseases. Disclosures: No relevant conflicts of interest to declare.
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Cattaneo, Maria Grazia, Sandra Pola, Valeria Dehò, Anna Maria Sanguini, and Lucia Maria Vicentini. "Alprostadil suppresses angiogenesis in vitro and in vivo in the murine Matrigel plug assay." British Journal of Pharmacology 138, no. 2 (January 2003): 377–85. http://dx.doi.org/10.1038/sj.bjp.0705051.

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7

M, Thiruselvi, and Brindha Durairaj. "IN VITRO AND IN VIVO ANTIANGIOGENIC EFFECT OF ARTOCARPUS HETEROPHYLLUS SEED EXTRACT." Asian Journal of Pharmaceutical and Clinical Research 11, no. 9 (September 7, 2018): 268. http://dx.doi.org/10.22159/ajpcr.2018.v11i9.27488.

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Objective: Angiogenesis the formation of new blood vessels from the pre-existing vasculature plays a major role in tumor growth, invasion, and metastasis of cancer diseases. The current research was designed for the inhibition of angiogenesis, which can provide a novel way to inhibit tumor growth and metastasis in cancer.Methods: The antiangiogenic properties of serial concentrations of the hydroethanolic extract of Artocarpus heterophyllus were examined in human umbilical vein endothelial cells (HUVECs) using a tube formation assay in vitro and in a Matrigel plug assay as in vivo model.Results: Hydroethanolic extract of A. heterophyllus significantly inhibited vascular endothelial growth factor (VEGF)-mediated angiogenesis in the HUVECs in culture dose-dependently. Further, the new blood vessel formation was observed to be inhibited by the extract at 100 mg/kg p.o. in Matrigel plug model in C57BL/6 mice. However, the effect was enhanced in higher concentration (500 mg/kg p.o.) demonstrating the in vivo antiangiogenic activity of the extract.Conclusion: This study demonstrated that the hydroethanolic seed extract of A. heterophyllus strongly inhibited the angiogenesis in HUVECs. Moreover, the extract significantly inhibited the VEGF production in HUVECs, confirming their possible antiangiogenic mechanism.
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Cheranov, Sergey Y., Dong Wang, Venkatesh Kundumani-Sridharan, Manjula Karpurapu, Qiuhua Zhang, Koteswara R. Chava, and Gadiparthi N. Rao. "The 15(S)-hydroxyeicosatetraenoic acid-induced angiogenesis requires Janus kinase 2-signal transducer and activator of transcription-5B–dependent expression of interleukin-8." Blood 113, no. 23 (June 4, 2009): 6023–33. http://dx.doi.org/10.1182/blood-2008-10-183210.

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Abstract To understand the molecular basis underlying 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE)–induced angiogenesis, we have studied the role of the Janus kinase-signal transducer and activator of transcription (Jak-STAT) signaling. The 15(S)-HETE stimulated tyrosine phosphorylation of Jak2 in a time-dependent manner in human retinal microvascular endothelial cells (HRMVECs). Inhibition of Jak2 activation via adenovirus-mediated expression of its dominant-negative mutant attenuated 15(S)-HETE–induced HRMVEC migration and tube formation and Matrigel plug angiogenesis. Similarly, 15(S)-HETE activated tyrosine phosphorylation of STAT-5B in a time-dependent manner. Dominant-negative mutant-mediated interference of STAT-5B activation suppressed 15(S)-HETE–induced HRMVEC migration and tube formation and Matrigel plug angiogenesis. The 15(S)-HETE induced interleukin-8 (IL-8) expression in Jak2-STAT-5B–dependent manner in HRMVECs. In addition, neutralizing anti–IL-8 antibodies reduced 15(S)-HETE–induced HRMVEC migration and tube formation and Matrigel plug angiogenesis. Cloning and Transfac analysis of IL-8 promoter revealed the presence of 1 putative STAT-binding sequence at −476 nt, and electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed the binding of STAT-5B to this site in response to 15(S)-HETE. Mutational analysis showed that STAT binding site is essential for 15(S)-HETE–induced IL-8 promoter activity. Together, these observations suggest that 15(S)-HETE–induced angiogenesis requires Jak2-STAT-5B–dependent expression of IL-8.
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9

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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Miyake, Makito, Steve Goodison, Evan Gomes, Wasia Rizwani, Shanti Ross, Ge Zhang, and Charles Joel Rosser. "Induction of endothelial proliferation and angiogenesis through activating the ERK1/2/EGF pathway mediate by CXC chemokine receptor 2 by chemokine (C-X-C motif) ligand 1." Journal of Clinical Oncology 31, no. 6_suppl (February 20, 2013): 138. http://dx.doi.org/10.1200/jco.2013.31.6_suppl.138.

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138 Background: Endothelial cell growth and proliferation are critical for tumoral angiogenesis. We report here that blockade of Chemokine (C-X-C motif) ligand 1 (CXCL1) results in reduction of human endothelial cell proliferation and its ability to induce angiogenesis. Methods: Two human endothelial cell lines, HUVEC and HDMEC, were used in the in vitro assays. Proliferation assay and matrigel tube formation assay were performed to test the inhibitory effect of anti-CXCL antibody on the activity of endothelial cells in vitro. Matrigel plug assay in nude mice was performed to test the in vivo angiogenic activity of CXCL1. Results: CXCL1 interacts with its receptor CXC chemokine Receptor 2 and induces endothelial cell proliferation, whereas blockade of CXCL1 is associated with reduction in cellular proliferation through a decrease in levels of cyclin D and cdk4 and inhibition of angiogenesis through EGF and ERK 1/2. Targeting CXCL1 inhibits neoangiogenesis but has no effect on disrupting established vasculature. Furthermore targeting CXCL1 is associated with reduction in migration of human endothelial cells in an in vitro model. Additionally, neutralizing antibody against CXCL1 in a xenograft angiogenesis model resulted in inhibition of angiogenesis. Conclusions: CXCL1-induced regulation of angiogenesis has not been studied extensively in human cancers, thus these findings illustrate a novel contribution of CXCL1 interactions in pathological angiogenesis. Therefore, the ability to selectively modulate CXCL1, specifically in tumoral angiogenesis, may promote the development of novel oncologic therapeutic strategies.
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Dissertations / Theses on the topic "Matrigel plug assay"

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Eubank, Tim. "M-CSF and GM-CSF induce human monocytes to express either pro- or anti-angiogenic factors." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1069772001.

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Rajashekhar, Gangaraju, Antje Willuweit, Carolyn E. Patterson, Peichuan Sun, Andreas Hilbig, Georg Breier, Armin Helisch, and Matthias Clauss. "Continuous Endothelial Cell Activation Increases Angiogenesis: Evidence for the Direct Role of Endothelium Linking Angiogenesis and Inflammation." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135425.

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There is increasing evidence that chronic inflammation is tightly linked to diseases associated with endothelial dysfunction, including the induction of aberrant angiogenesis. While leukocytes have been described as mediators of inflammation-associated angiogenesis, the effects of direct chronic endothelial activation have not been addressed in this context. Using an uncleavable mutant of the transmembrane form of tumor necrosis factor-α (TNF-α), we have established models of stable TNF-α expression in endothelial cells in vitro and in transgenic mice in vivo. In the in vitro model, continuous endothelial activation leads to increased leukocyte cellular adhesion molecule expression and intracellular reactive oxygen species, hallmarks of a proinflammatory and dysfunctional endothelium. In addition, stable expression of TNF-α in endothelial cells increased angiogenic sprout formation in the presence but also in the absence of angiogenic growth factors. The partial neutralization of this effect by TNF-α antibodies and the inability of conditioned media from stable TNF-α-expressing endothelial cells to induce angiogenic activities in control endothelial cells suggest that this effect does not require expression of additional autocrine factors, but is an autonomous effect of the transmembrane TNF on the endothelial cells. Furthermore, using the Matrigel plug assay in vivo, increased angiogenesis was observed in endothelial TNF-α-expressing transgenic versus control mice. In conclusion, chronic inflammatory changes mediated by TNF-α can induce angiogenesis in vitro and in vivo, suggesting endothelial cell activation as a direct link between inflammation and angiogenesis
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
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3

Rajashekhar, Gangaraju, Antje Willuweit, Carolyn E. Patterson, Peichuan Sun, Andreas Hilbig, Georg Breier, Armin Helisch, and Matthias Clauss. "Continuous Endothelial Cell Activation Increases Angiogenesis: Evidence for the Direct Role of Endothelium Linking Angiogenesis and Inflammation." Karger, 2006. https://tud.qucosa.de/id/qucosa%3A27647.

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There is increasing evidence that chronic inflammation is tightly linked to diseases associated with endothelial dysfunction, including the induction of aberrant angiogenesis. While leukocytes have been described as mediators of inflammation-associated angiogenesis, the effects of direct chronic endothelial activation have not been addressed in this context. Using an uncleavable mutant of the transmembrane form of tumor necrosis factor-α (TNF-α), we have established models of stable TNF-α expression in endothelial cells in vitro and in transgenic mice in vivo. In the in vitro model, continuous endothelial activation leads to increased leukocyte cellular adhesion molecule expression and intracellular reactive oxygen species, hallmarks of a proinflammatory and dysfunctional endothelium. In addition, stable expression of TNF-α in endothelial cells increased angiogenic sprout formation in the presence but also in the absence of angiogenic growth factors. The partial neutralization of this effect by TNF-α antibodies and the inability of conditioned media from stable TNF-α-expressing endothelial cells to induce angiogenic activities in control endothelial cells suggest that this effect does not require expression of additional autocrine factors, but is an autonomous effect of the transmembrane TNF on the endothelial cells. Furthermore, using the Matrigel plug assay in vivo, increased angiogenesis was observed in endothelial TNF-α-expressing transgenic versus control mice. In conclusion, chronic inflammatory changes mediated by TNF-α can induce angiogenesis in vitro and in vivo, suggesting endothelial cell activation as a direct link between inflammation and angiogenesis.
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
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Book chapters on the topic "Matrigel plug assay"

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Kastana, Pinelopi, Fatema Tuz Zahra, Despoina Ntenekou, Stamatiki Katraki-Pavlou, Dimitris Beis, Michail S. Lionakis, Constantinos M. Mikelis, and Evangelia Papadimitriou. "Matrigel Plug Assay for In Vivo Evaluation of Angiogenesis." In The Extracellular Matrix, 219–32. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9133-4_18.

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Conference papers on the topic "Matrigel plug assay"

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Sun, Yanmei, Xiaoming Song, Nan Li, Jie Cai, Qian Shi, and Taiping Chen. "Abstract 1614: Murine matrigel plug assay for quick evaluation of anti-angiogenesis drugs." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1614.

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