Relevant bibliographies by topics / Chemokine SDF-1

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  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Chemokine SDF-1'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Chemokine SDF-1"

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Rabkin, Charles S., Quan-en Yang, James J. Goedert, Giao Nguyen, Hiroaki Mitsuya, and Shizuko Sei. "Chemokine and Chemokine Receptor Gene Variants and Risk of Non-Hodgkin’s Lymphoma in Human Immunodeficiency Virus-1–Infected Individuals." Blood 93, no. 6 (March 15, 1999): 1838–42. http://dx.doi.org/10.1182/blood.v93.6.1838.406k39_1838_1842.

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Normal B-lymphocyte maturation and proliferation are regulated by chemotactic cytokines (chemokines), and genetic polymorphisms in chemokines and chemokine receptors modify progression of human immunodeficiency virus-1 (HIV-1) infection. Therefore, 746 HIV-1–infected persons were examined for associations of previously described stromal cell-derived factor 1 (SDF-1) chemokine and CCR5 and CCR2 chemokine receptor gene variants with the risk of B-cell non-Hodgkin’s lymphoma (NHL). The SDF1-3′A chemokine variant, which is carried by 37% of whites and 11% of blacks, was associated with approximate doubling of the NHL risk in heterozygotes and roughly a fourfold increase in homozygotes. After a median follow-up of 11.7 years, NHL developed in 6 (19%) of 30 SDF1-3′A/3′A homozygotes and 22 (10%) of 202 SDF1-+/3′A heterozygotes, compared with 24 (5%) of 514 wild-type subjects. The acquired immunodeficiency syndrome (AIDS)-protective chemokine receptor variant CCR5-▵32 was highly protective against NHL, whereas the AIDS-protective variant CCR2-64I had no significant effect. Racial differences in SDF1-3′A frequency may contribute to the lower risk of HIV-1–associated NHL in blacks compared with whites. SDF-1 genotyping of HIV-1–infected patients may identify subgroups warranting enhanced monitoring and targeted interventions to reduce the risk of NHL.
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Ho, Teik K., X. Shiwen, D. Abraham, J. Tsui, and D. Baker. "Stromal-Cell-Derived Factor-1 (SDF-1)/CXCL12 as Potential Target of Therapeutic Angiogenesis in Critical Leg Ischaemia." Cardiology Research and Practice 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/143209.

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In the Western world, peripheral vascular disease (PVD) has a high prevalence with high morbidity and mortality. In a large percentage of these patients, lower limb amputation is still required. Studies of ischaemic skeletal muscle disclosed evidence of endogenous angiogenesis and adaptive skeletal muscle metabolic changes in response to hypoxia. Chemokines are potent chemoattractant cytokines that regulate leukocyte trafficking in homeostatic and inflammatory processes. More than 50 different chemokines and 20 different chemokine receptors have been cloned. The chemokine stromal-cell-derived factor-1 (SDF-1 aka CXCL12) is a constitutively expressed and inducible chemokine that regulates multiple physiological processes, including embryonic development and organ homeostasis. The biologic effects of SDF-1 are mediated by chemokine receptor CXCR4, a 352 amino acid rhodopsin-like transmembrane-specific G protein-coupled receptor (GPCR). There is evidence that the administration of SDF-1 increases blood flow and perfusion via recruitment of endothelial progenitor cells (EPCs). This review will focus on the role of the SDF-1/CXCR4 system in the pathophysiology of PVD and discuss their potential as therapeutic targets for PVD.
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Stumm, Ralf, and Volker Höllt. "CXC chemokine receptor 4 regulates neuronal migration and axonal pathfinding in the developing nervous system: implications for neuronal regeneration in the adult brain." Journal of Molecular Endocrinology 38, no. 3 (March 2007): 377–82. http://dx.doi.org/10.1677/jme-06-0032.

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Chemotactic cytokines (chemokines) are small secreted proteins that control leukocyte trafficking in immune organs. Chemokines which are induced in the brain during conditions of inflammation play a role in the local immune response. Recently, it has been established in the rodent brain that distinct chemokines and chemokine receptors are constitutively expressed by neurons and that these chemokines modulate neuronal functions. The CXC motif chemokine stromal cell-derived factor-1 (SDF-1), CXCL12 together with its cognate receptor CXCR4 represents the best-characterized neuronal chemokine system. Transwell migration assays with neuronal precursors, pharmacological manipulation of CXCR4 signaling in embryonic brain explants, and histochemical studies of SDF-1- or CXCR4-deficient mouse embryos provide proof that SDF-1 directs neuronal migration and axonal pathfinding in the developing nervous system. In the adult brain, SDF-1 is thought to influence neurogenesis as well as recruitment of brain resident and non-resident circulating cells toward sites of lesion. The present review summarizes patterns and functions of the SDF-1/CXCR4 system in the rodent brain with a focus on the developing and adult cerebral cortex.
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Tilton, Bettina, Liza Ho, Estelle Oberlin, Pius Loetscher, Françoise Baleux, Ian Clark-Lewis, and Marcus Thelen. "Signal Transduction by Cxc Chemokine Receptor 4." Journal of Experimental Medicine 192, no. 3 (July 31, 2000): 313–24. http://dx.doi.org/10.1084/jem.192.3.313.

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We report that stromal cell–derived factor (SDF)-1 has the remarkable capacity to induce sustained signaling through CXC chemokine receptor 4 (CXCR4). In contrast to other chemokines, such as monocyte chemotactic protein 1 (CC chemokine receptor 2 [CCR2]), macrophage inflammatory protein 1β (CCR5), liver and activation-regulated chemokine (LARC [CCR6]), Epstein-Barr virus–induced molecule 1 ligand chemokine (ELC [CCR7]), and IP10 (CXCR3), SDF-1 stimulates the prolonged activation of protein kinase B and extracellular signal–regulated kinase (ERK)-2. Activation of protein kinase B is reversed by displacement of SDF-1 from CXCR4 or inhibition of phosphatidylinositol 3-kinase. Although increasing concentrations of SDF-1 enhance CXCR4 internalization, kinase activation is prolonged. In addition, restimulation yields >60% of initial protein kinase B activity, indicating that the remaining receptors are not desensitized. Furthermore, activation is prolonged by inhibiting SDF-1 degradation. The sustained activation of cell survival and mitogenic pathways may account for the unique role of SDF-1 and CXCR4 in embryogenesis and lymphopoiesis.
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Perks, Bea. "SDF-1: the repulsive chemokine." Immunology Today 21, no. 7 (July 2000): 309. http://dx.doi.org/10.1016/s0167-5699(00)01685-6.

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Kowalska, M. Anna, Mariusz Z. Ratajczak, Marcin Majka, Jianguo Jin, Satya Kunapuli, Lawrence Brass, and Mortimer Poncz. "Stromal cell–derived factor-1 and macrophage-derived chemokine: 2 chemokines that activate platelets." Blood 96, no. 1 (July 1, 2000): 50–57. http://dx.doi.org/10.1182/blood.v96.1.50.

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Abstract Platelets play roles in both thrombosis and inflammation, and chemokines that are released at sites of inflammation could potentially activate platelets. Among the chemokine receptors expressed on platelets, the CXCR4 is the receptor for chemokine stromal cell-derived factor-1 (SDF-1), and the CCR4 is the receptor for macrophage-derived chemokine (MDC). Of the chemokines tested, SDF-1 and MDC were the only 2 that activated platelets. Both are weak agonists, but they enhanced response to low-dose adenosine 5′-diphosphate (ADP), epinephrine, or serotonin. When SDF-1 and MDC were added together, full and brisk platelet aggregation occurred. Platelet activation by these 2 chemokines appears to involve distinct pathways: SDF-1 inhibited an increase in cyclic adenosine monophosphate (cAMP) following prostaglandin (PG) I2, while MDC had no effect. In contrast, MDC, but not SDF-1, lead to Ca++mobilization by platelets. Further, second-wave aggregation induced by MDC in platelet-rich plasma was inhibited by aspirin, ADP scavenger creatine phosphate/creative phosphokinase (CP/CPK), and ARL-66096, an antagonist of the ADP P2TAC receptor involved in adenylyl cyclase inhibition. But the aggregation was not affected by A3P5PS, an inhibitor of the ADP P2Y receptor. SDF-1–induced aggregation was inhibited by aspirin, but it was only slightly affected by CP/CPK, ARL-66096, or A3P5PS. Finally, the presence of chemokines in platelets was determined. Reverse transcriptase–polymerase chain reaction studies with platelet RNA did not detect the presence of SDF-1 or MDC. In summary, SDF-1 and MDC are platelet agonists that activate distinct intracellular pathways. Their importance in the development of thrombosis at sites of inflammation needs to be further evaluated.
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Kowalska, M. Anna, Mariusz Z. Ratajczak, Marcin Majka, Jianguo Jin, Satya Kunapuli, Lawrence Brass, and Mortimer Poncz. "Stromal cell–derived factor-1 and macrophage-derived chemokine: 2 chemokines that activate platelets." Blood 96, no. 1 (July 1, 2000): 50–57. http://dx.doi.org/10.1182/blood.v96.1.50.013k40_50_57.

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Platelets play roles in both thrombosis and inflammation, and chemokines that are released at sites of inflammation could potentially activate platelets. Among the chemokine receptors expressed on platelets, the CXCR4 is the receptor for chemokine stromal cell-derived factor-1 (SDF-1), and the CCR4 is the receptor for macrophage-derived chemokine (MDC). Of the chemokines tested, SDF-1 and MDC were the only 2 that activated platelets. Both are weak agonists, but they enhanced response to low-dose adenosine 5′-diphosphate (ADP), epinephrine, or serotonin. When SDF-1 and MDC were added together, full and brisk platelet aggregation occurred. Platelet activation by these 2 chemokines appears to involve distinct pathways: SDF-1 inhibited an increase in cyclic adenosine monophosphate (cAMP) following prostaglandin (PG) I2, while MDC had no effect. In contrast, MDC, but not SDF-1, lead to Ca++mobilization by platelets. Further, second-wave aggregation induced by MDC in platelet-rich plasma was inhibited by aspirin, ADP scavenger creatine phosphate/creative phosphokinase (CP/CPK), and ARL-66096, an antagonist of the ADP P2TAC receptor involved in adenylyl cyclase inhibition. But the aggregation was not affected by A3P5PS, an inhibitor of the ADP P2Y receptor. SDF-1–induced aggregation was inhibited by aspirin, but it was only slightly affected by CP/CPK, ARL-66096, or A3P5PS. Finally, the presence of chemokines in platelets was determined. Reverse transcriptase–polymerase chain reaction studies with platelet RNA did not detect the presence of SDF-1 or MDC. In summary, SDF-1 and MDC are platelet agonists that activate distinct intracellular pathways. Their importance in the development of thrombosis at sites of inflammation needs to be further evaluated.
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Maréchal, Valérie, Fernando Arenzana-Seisdedos, Jean-Michel Heard, and Olivier Schwartz. "Opposite Effects of SDF-1 on Human Immunodeficiency Virus Type 1 Replication." Journal of Virology 73, no. 5 (May 1, 1999): 3608–15. http://dx.doi.org/10.1128/jvi.73.5.3608-3615.1999.

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ABSTRACT The α-chemokine SDF-1 binds CXCR4, a coreceptor for human immunodeficiency virus type 1 (HIV-1), and inhibits viral entry mediated by this receptor. Since chemokines are potent chemoattractants and activators of leukocytes, we examined whether the stimulation of HIV target cells by SDF-1 affects the replication of virus with different tropisms. We observed that SDF-1 inhibited the entry of X4 strains and increased the infectivity of particles bearing either a CCR5-tropic HIV-1 envelope or a vesicular stomatitis virus G envelope. In contrast to the inhibitory effect of SDF-1 on X4 strains, which is at the level of entry, the stimulatory effect does not involve envelope-receptor interactions or proviral DNA synthesis. Rather, we observed an increased ability of Tat to transactivate the HIV-1 long terminal repeat in the presence of the chemokine. Therefore, the effects of SDF-1 on the HIV-1 life cycle can be multiple and opposite, including both an inhibition of viral entry and a stimulation of proviral gene expression.
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Miura, Kohei, Shashi Uniyal, Mircea Leabu, Tamas Oravecz, Subrata Chakrabarti, Vincent L. Morris, and Bosco M. C. Chan. "Chemokine receptor CXCR4-β1 integrin axis mediates tumorigenesis of osteosarcoma HOS cells." Biochemistry and Cell Biology 83, no. 1 (February 1, 2005): 36–48. http://dx.doi.org/10.1139/o04-106.

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It is known that β1 integrins mediate the migratory response of cells to chemokine stimulation. Also, both β1 integrins and chemokines have roles in tumor development. In the present study, the β1 integrin-chemokine axis is assessed using human osteosarcoma (HOS) transfectant cells expressing the CXCR4 receptor for chemokine SDF-1 (CXCL12). We first identified in vitro the specific β1 integrins that mediated the migratory response to SDF-1 stimulation. Results showed that on collagen type I and laminin, the chemotactic response to SDF-1 was predominantly mediated by α2β1 integrin. On fibronectin, SDF-1-stimulated chemotaxis involved both α4β1 and α5β1 integrins. A comparison of the transfectant clones expressing CXCR4 at low, intermediate, and high levels and the control transfectant revealed that the transfectant clones migratory response in vitro and their ability to form tumors in vivo was related to their levels of CXCR4 expression. In addition, treatment by injection with mAbs to CXCR4, integrin α2β1, or integrin α5β1 effectively inhibited the growth of HOS-CXCR4 transfectant cells in vivo. Therefore, our results show that the β1 integrins that mediated the migratory response were also functionally linked to the enhanced tumor growth of CXCR4-expressing HOS transfectant cells.Key words: integrins, chemokines, chemotaxis, osteosarcoma, tumorigenesis.
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Gear, Adrian R. L., Sudawadee Suttitanamongkol, Delia Viisoreanu, Renata K. Polanowska-Grabowska, Sanghamitra Raha, and David Camerini. "Adenosine diphosphate strongly potentiates the ability of the chemokines MDC, TARC, and SDF-1 to stimulate platelet function." Blood 97, no. 4 (February 15, 2001): 937–45. http://dx.doi.org/10.1182/blood.v97.4.937.

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Abstract Platelet activation is normally induced by primary agonists such as adenosine diphosphate (ADP), thrombin, and collagen, whereas other agonists, such as epinephrine, can play important accessory roles. It is now reported that the macrophage-derived chemokine (MDC), thymus activation–regulated chemokine (TARC), and stromal cell–derived factor one (SDF-1) are highly effective activators of platelet function under a variety of conditions, stimulating platelet shape change, aggregation, and adhesion to collagen or fibrinogen. Chemokine-mediated platelet activation was rapid and maximal (less than 5 seconds) under arterial flow conditions and depended strongly on the presence of low levels of primary agonists such as ADP or thrombin. Concentrations of ADP (0.05-0.25 μM) or thrombin (0.005-0.02 U/mL) that induced minimal aggregation caused major aggregation acting in combination with the chemokines. The ability of apyrase to block chemokine-dependent aggregation or adhesion was consistent with an important role for ADP. Chemokine-stimulated aggregation was also insensitive to indomethacin, suggesting that the activation of cyclo-oxygenase is not involved. TARC, MDC, and SDF-1 increased intracellular calcium concentrations [Ca2+]iwhen combined with low levels of ADP. The MDC and TARC receptor CCR4 was expressed on platelets, and an anti-CCR4 antibody blocked aggregation induced by TARC or MDC. Treatment of platelets with SDF-1 and MDC rapidly exposed P-selectin (CD62P) on the cell surface but did not induce the secretion of serotonin. These findings suggest that the chemokines MDC, TARC, and SDF-1, which may be produced during inflammatory responses, coupled with low levels of ADP or thrombin, can serve as strong stimuli for activating platelet function.
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Dissertations / Theses on the topic "Chemokine SDF-1"

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Cavalcante, GalylÃia Menezes. "Study of expression of systems CXCR4-CXCL12/SDF-1, CCR7-CCL21 and Ki-67 in the oral squamous cell carcinoma and their association with clinicopathological factors,nodal metastases and survival." Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11989.

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Chemokines are responsible for the directed migration of leukocyte chemotactic cytokines, coordinating cell movement during inflammation and the transport of hematopoietic cells. In addition to leukocytes, chemokine receptors are also found in neoplastic cells and tumors associated with stromal cells. Among chemokines, and the CXCR4/CXCL12 CCR7/CCL21 systems have been shown the involvement of lymph node metastases or distant metastases in different cancers. Thus, aim of this study was to evaluate the expression of CXCR4, CXCL12, CCR7, CCL21 and Ki-67 in oral squamous cell carcinoma (SCC) and to correlate these markers with clinicopathological indicators, lymph node metastasis and survival. We conducted a survey of reports and paraffin blocks of excisional biopsies of patients with SCC treated at the Hospital Haroldo JuaÃaba (2001-2009). Data on anatomic location of the lesion, sex, age, patient survival, degree of histological differentiation of the tumor, tumor stage and presence or absence of lymph node metastasis, lymphovascular and perineural invasion, nuclear grade and depth of invasion were collected. For immunohistochemical analysis, followed by the technique of streptavidin-biotin-peroxidase using the anti-CXCR4, anti-CXCL12, anti-CCR7, anti-CCL21 and Ki-67 antibody. Histological sections were photomicrographed in 10 fields chosen randomly and measured for the number of labeled tumor cells and determined the percentage of each labeling antibody. The marking of CXCR4 was detected in the cytoplasm and nucleus, CXCL12, CCR7 and CCL21 were only cytoplasmic, their expression was observed in 18 (60%) 8 (22.66%) 16 (53.3%) and 3 (12%) cases, respectively. We found a significant positive association between lymphovascular invasion and immunostaining of CXCR4 (p = 0.007) and CCR7 (P = 0.01) and among these cases metastasis was present in 62.5% and 37.5%, respectively. When in combination with Ki67, we found a significant positive correlation between CXCR4 (p = 0.0086), CXCL12 (p = 0.036) and CCR7 (p = 0:04). Among patients CXCR4 + over 111 months, only 38.4% were alive (p = 0.845), whereas both patients CCR7 + (p = 0.398) as well as CXCR4 +, and CCR7 + (p = 0.441) after 62 months, everyone had already died. We conclude that these chemokines are associated with lymphovascular invasion and cell proliferation, perhaps favoring the development of metastasis and poor prognosis.
As quimiocinas sÃo citocinas quimiotÃticas responsÃveis pela migraÃÃo direcionada de leucÃcitos, coordenando o movimento celular durante a inflamaÃÃo e o transporte de cÃlulas hematopoiÃticas. AlÃm dos leucÃcitos, os receptores de quimiocinas tambÃm sÃo encontrados em cÃlulas neoplÃsicas e em tumores associados com cÃlulas estromais. Dentre as quimiocinas, os sistemas CXCR4/CXCL12 e CCR7/CCL21 tÃm sido demonstrado no envolvimento de metÃstases linfonodais ou à distÃncia em diferentes tipos de cÃncer. Dessa forma, foi objetivo desse trabalho avaliar a expressÃo de CXCR4, CXCL12, CCR7, CCL21 e Ki-67 em carcinoma de cÃlulas escamosas orais (CEC) e correlacionar estes marcadores com indicadores clÃnicopatolÃgicos, metÃstase linfonodal e sobrevida. Realizou-se um levantamento de laudos e blocos parafinados de biopsias excisionais de pacientes portadores de CEC tratados no Hospital Haroldo JuaÃaba (2001 a 2009). Foram coletados dados sobre localizaÃÃo anatÃmica da lesÃo, sexo, idade, sobrevida do paciente, grau de diferenciaÃÃo histopatolÃgica do tumor, estadiamento tumoral e presenÃa ou ausÃncia de metÃstase linfonodal, invasÃo linfovascular e perineural, grau nuclear e profundidade de invasÃo. Para reaÃÃo de imunohistoquÃmica, seguiu-se a tÃcnica da estreptavidina-biotina-peroxidase, utilizando os anticorpos anti-CXCR4, anti-CXCL12, anti-CCR7, anti-CCL21 e Ki-67. As secÃÃes histolÃgicas foram fotomicrografadas em 10 campos escolhidos aleatoriamente e quantificadas quanto ao nÃmero de cÃlulas tumorais marcadas e determinado o percentual de marcaÃÃo de cada anticorpo. A marcaÃÃo de CXCR4 foi detectada em citoplasma e nÃcleo, CXCL12, CCR7 e CCL21 tiveram marcaÃÃo apenas citoplasmÃtica, sendo observada suas expressÃes em 18 (60%), 8 (22,66%), 16 (53,3%) e 3 (12%) casos, respectivamente. Encontrou-se uma associaÃÃo significativa positiva entre a invasÃo linfovascular e a imunomarcaÃÃo do CXCR4 (p=0.007) e CCR7 (p=0.01) e dentre esses casos a metÃstase esteve presente em 62,5% e 37,5%, respectivamente. Quando em associaÃÃo com o Ki67, encontrou-se uma correlaÃÃo positiva significante entre o CXCR4 (p=0.0086), CXCL12 (p=0.036) e CCR7 (p=0.04). Dentre os pacientes CXCR4+, ao longo de 111 meses, apenas 38,4% estavam vivos (p=0.845), ao passo que tanto para pacientes CCR7+ (p = 0.398), quanto CXCR4+ e CCR7+ (p = 0.441), apÃs 62 meses, todos haviam ido a Ãbito. Conclui-se que essas quimiocinas estÃo associadas com a invasÃo linfovascular e proliferaÃÃo celular, talvez favorecendo o desenvolvimento de metÃstases e um pior prognÃstico.
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Memi, F. "The role of the chemokine SDF-1 and its receptors CXCR4 and CXCR7 in the migration of GnRH neurons." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1388706/.

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Reproduction in mammals is initiated and maintained by a small population of cells called Gonadotropin-releasing hormone (GnRH) neurons, scattered throughout the preoptic area and anterior hypothalamus. These neurons originate in the nasal placode, and migrate across the nasal compartment in association with olfactory, vomeronasal and terminal nerves to reach their targets in the hypothalamus. In humans, defective GnRH neuron migration results in gonadal dysfunction and subsequent infertility. As mutated genes identified so far in patients account for only 30% of the cases, many unknown genes involved in GnRH neuron development still need to be discovered. One of the molecules required for their early migration is the chemokine SDF-1 which is expressed in the embryonic nasal mesenchyme in an increasing rostral to caudal gradient, presumably guiding CXCR4-expressing GnRH neurons towards the forebrain. Mice lacking CXCR4, the receptor for SDF-1, exhibit defective GnRH neuron migration along with a significant reduction in number. This thesis focuses on the role of the more recently identified second SDF-1 receptor, CXCR7, in GnRH neuron development. A detailed analysis of the expression pattern of CXCR7 in the nasal region and comparison to that of its agonist (SDF-1) as well as CXCR4, was elucidated for the first time. CXCR7 was found to be expressed along the migratory path of GnRH neurons in the nasal region, but not by GnRH neurons or their guiding axons. The role of CXCR7 in GnRH neuron migration in vivo was assessed using transgenic mice deficient for this receptor. This analysis revealed that in these mice, many GnRH cells remained in the nasal compartment, clustering or found ectopically in the olfactory epithelium. Interestingly, CXCR4 was downregulated in CXCR7 defective mice, suggesting that CXCR7 affects GnRH migration indirectly, by regulating CXCR4 in a non-cell autonomous manner.
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Reinhold, Lars Henning. "Einfluss von SDF 1-[alpha] [1-Alpha] auf den Ca2+-aktivierten K+-Kanal mit grosser Leitfähigkeit und die daraus resultierenden Auswirkungen auf die Proliferation, Migration, NO- und Ca2+-Homöostase humaner Endothelzellen." Giessen VVB Laufersweiler, 2007. http://d-nb.info/991416503/04.

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Oliveira, Adriana Morgan de. "Expressão da quimiocina SDF-1, (CXCL12) e seu respectivo receptor CXCR4 em células de pacientes com mieloma múltiplo em linhagem de células mieloma múltiplo humano (RPMI-8226) após tratamento com talidomida." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-30102008-145739/.

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Mieloma Múltiplo é a segunda doença com maior prevalência nas doenças malignidades hematológica, incurável com média de sobrevivência de 3-5 anos. MM é uma malignidade das células do plasma caracterizada pela destruição e reabsorção óssea e supressão da formação do osso. A quimiocina SDF-1 (CXCL12) e seu receptor CXCR4 têm um importante papel direcional na migração, homing das células do plasma em mieloma múltiplo e mobilização das células de MM para fora da medula óssea. A talidomida tem sido usada com êxito no tratamento de pacientes com mieloma múltiplo. Neste estudo verificamos o efeito da talidomida na expressão da quimiocina SDF-1 e seu receptor CXCR4 em pacientes com mieloma múltiplo e em linhagem de células de mieloma múltiplo humano (RPMI-8226) tratados e sem tratamento de talidomida. Nossos resultamos mostraram uma expressão heterogênea na expressão da quimiocina SDF-1 e seu receptor CXCR4 nos pacientes com mieloma múltiplo estudado (n= 79). Entretanto, pacientes com mieloma múltiplo tratados com talidomida mostraram uma baixa expressão da quimiocina SDF-1 e seu receptor CXC4 quando comparados com pacientes recém diagnosticados para mieloma múltiplo e pacientes com mieloma múltiplo tratados com outros medicamentos. Nossos resultados sugerem que o tratamento com talidomida induz uma baixa regulação na expressão no ligante SDF-1 e seu receptor CXCR4 em pacientes com mieloma múltiplo
Multiple Myeloma (MM) is a second most prevalent hematological malignancy and remains incurable with a median survival of 3-5 years. MM is a plasma cell malignancy characterized by devastating bone destruction due to the enhanced bone resorption and suppressed bone formation. The chemokine stromal-derived factor-1 (SDF-1) and its receptor CXCR4 play an important role in directional migration, homing of plasma cells in multiple myeloma (MM) and mobilization of MM cells out of the bone marrow. The drug thalidomide has been successfully used in the treatment of patients with MM. In this study, we assessed the effect of thalidomide on SDF-1 and CXCR4 expression in MM patients and human myeloma-derived cell line, RPMI 8226 treated with or without thalidomide. A heterogeneous expression pattern of chemokines SDF-1 and CXCR4 receptor were observed for all MM patients studied. However, patients treated with thalidomide showed a significantly decrease in expression of SDF-1 and CXCR4 as compared to newly diagnosed MM patients and MM patients treated with other drugs. RPMI 8226 cell line treated with 10, 20 and 100µM thalidomide also demonstrated decrease in SDF-1 and CXCR4 expression as compared with cell control (RPMI-8226 without thalidomide). Ours results indicate that thalidomide therapy induces down-regulation of CXCR4 and its ligand SDF-1 in multiple myeloma
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Czardybon, Margarete. "Charakterisierung der Genexpression des neuen Chemokines SDF-1[gamma] [SDF-1gamma] im Nervensystem der Ratte." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=966046552.

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Cramer, Manuela J. "Das Chemokin SDF-1[alpha] [SDF-1-alpha] interferiert mit der IL-2-induzierten T-Zell-Proliferation Beschreibung eines neuen regulatorischen Mechanismus." Karlsruhe FZKA, 2005. http://bibliothek.fzk.de/zb/berichte/FZKA7202.pdf.

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Sipert, Carla Renata. "Produção de MIP-1alfa e SDF-1 por fibroblastos de polpa dental humana em cultura frente ao desafio com Enterococcus faecalis inativado por calor." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/25/25138/tde-15102008-164844/.

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A polpa dental é formada de tecido conjuntivo frouxo sendo constituída por diversas células, dentre as quais os fibroblastos são as mais numerosas. Ao serem submetidas a agressões diversas, estas células respondem com a liberação de substâncias, tais como citocinas e quimiocinas, que participam de maneira ativa no processo inflamatório. Assim sendo, este trabalho teve como proposição: 1. avaliar a capacidade de fibroblastos de polpa dental humana em cultura em produzirem as quimiocinas MIP-l\'alfa\' /CCL3 e SDF-1/CXCL12; 2. avaliar a produção destas quimiocinas pelos fibroblastos quando estimulados por Enterococcus faecalis morto por calor com relação à quantidade de bactérias por célula e 3. avaliar a liberação destas quimiocinas com relação ao tempo de estímulo. Para o estabelecimento das culturas, foi coletada a polpa de terceiro molar hígido de um paciente saudável. O tecido foi extraído, armazenado e picotado em meio de cultura para fibroblastos (DMEM), os quais foram utilizados a partir da quarta passagem. Após adesão das células a placas de 24 poços, o meio de cultura contendo Enterococcus .faecalis morto por calor numa concentração correspondente a 1, 10 e 100 bactérias por fibroblasto foi adicionado aos poços. Após 1, 6 e 24 horas, o sobrenadante das células foi coletado para a análise por ELISA. A análise estatística foi realizada aplicando-se o teste Kruskal-Wallis com nível de significância de 5%. A produção de MIP-l\'alfa\' /CCL3 e SDF-l/CXCL12 pelas células pôde ser detectada por ELISA. Os fibroblastos pulpares se mostraram capazes de produzir SDF-1 constitutivamente sendo que o estímulo bacteriano levou a uma diminuição estatisticamente significativa desta produção. A produção de MIP-l\'alfa\' também foi detectada tanto de maneira constitutiva como em resposta ao desafio microbiano. Enquanto a concentração intermediária de bactéria por fibroblasto (10:1) mostrou uma produção semelhante ao grupo controle, as concentrações de 1 e 100 bactérias por fibroblasto induziram aumento maior na primeira hora de estímulo. Essas diferenças, entretanto, não foram estatisticamente significativas. A capacidade dos fibroblastos secretarem quimiocinas, como MIP-l\'alfa\' e SDF-1, reforça a importância dessas células dentro do contexto de imunidade e inflamação pulpar, principalmente por serem as células mais numerosas deste microambiente.
Dental pulp is a connective tissue structure constituted by many different cell types. Among them, the fibroblasts are the most frequent ones. When challenged by different aggressive agents, these cells are able to release some substances like cytokines and chemokines, which are essential to trigger the inflammatory process. The aims of this study were: 1. to evaluate the ability of fibroblasts to produce the chemokines MIP-l\'alfa\'/CCL3) and SDF-1/CXCL12; 2. to evaluate the expression of these chemokines by fibroblasts when challenged by heat killed Enterococcus. faecalis in gradual concentrations and 3. to evaluate the production of these chemokines in a time course manner. The dental pulp from non-carious third molar was collected from a healthy patient. Explants were made and stocked in culture medium (DMEM) for fibroblasts growth. The cells were used since passage four. In a 24-well plate and after reaching confluence, culture medium alone or containing heat killed E. faecalis at proportion 1:1, 10:1 and 100:1 bacteria:fibroblast, were added to the fibroblasts. After 1, 6 and 24 hours, the supernatants were collected for analysis. The protein detection of MIP-l\'alfa\'/CCL3 and SDF-1/CXCL12 was performed by ELISA. For statistical analysis, data were assessed by Kruskal-Wallis followed by Miller post-test. Significance levels of 5% were adopted. Production of both chemokines was detected by ELISA. Pulp fibroblasts were able to produce SDF-1 constitutively. This production decreased with the increase in the number of heat killed E. faecalis increased (p < 0.05). Production of MIP-l\'alfa\' was detected in unchallenged and challenged cells. The median bacterial concentration (10:1) presented a profile production similar to that of unstimulated cells. Bacterial concentrations of 1 and 100 microrganisms/cell showed a highly enhanced production of MIP-l\'alfa\' at the first hour of stimulum; however, these data were not statistically significant (p > 0.05). Fibroblasts ability to produce chemokines, like MIP-l\'alfa\' and SDF-1, confirms their importance at immune and inflammatory events in dental pulp, specially being fibroblasts the most abundant cells at this microenvironment .
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Cramer, Manuela J. [Verfasser]. "Das Chemokin SDF-1α [SDF-1-alpha] interferiert mit der IL-2-induzierten T-Zell-Proliferation : Beschreibung eines neuen regulatorischen Mechanismus / Forschungszentrum Karlsruhe GmbH, Karlsruhe. Manuela J. Cramer." Karlsruhe : FZKA, 2006. http://d-nb.info/980147905/34.

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Spoo, Anke. "Die Bedeutung der Interaktion des Chemokins SDF-1 (CXCL12) mit CXCR4-Chemokinrezeptoren auf Leukämiezellen von Patienten mit Akuter Myeloischer Leukämie." [S.l. : s.n.], 2004. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB11244028.

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Tzeng, Yi-Shiuan, and 曾奕軒. "Investigation of regulatory mechanism of chemokine CXCL12/SDF-1 in adult hematopoietic stem/progenitor cells homeostasis." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/77507667449904007819.

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博士
國立陽明大學
生化暨分子生物研究所
99
The C-X-C-type chemokine CXCL12, also known as Stromal cell-Derived Factor-1 (SDF-1), plays a critical role in hematopoiesis during fetal development. However, the functional requirement of CXCL12 in the adult hematopoietic stem/progenitor cell (HSPC) regulation was still unclear. In this thesis, a murine CXCL12 conditional deletion model was generated in which the target gene can be deleted at the adult stage. I found that loss of stroma-secreted CXCL12 in the adult led to expansion of the HSPC population as well as a reduction in long-term quiescent stem cells. In CXCL12-deficient bone marrow (BM), HSPCs were absent along the endosteal surface and blood cell regeneration occurred predominantly in the peri-sinusoidal space after the 5-fluorouracil myelosuppression challenge. The results indicate that CXCL12 is required for HSPC homeostasis regulation and is an important factor for osteoblastic niche organization in adult stage BM.
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Book chapters on the topic "Chemokine SDF-1"

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Lapidot, T. "The Roles of the Chemokine SDF-1 and its Receptor CXCR4 in Human Stem Cell Migration and Repopulation of NOD/SCID and B2mnull NOD/SCID mice." In Transplantation in Hematology and Oncology II, 11–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55774-3_2.

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Nagasawa, Takashi, Kazunobu Tachibana, and Kenji Kawabata. "A CXC Chemokine SDF-1/PBSF: A Ligand for a HIV Coreceptor, CXCR4." In Advances in Immunology, 211–28. Elsevier, 1998. http://dx.doi.org/10.1016/s0065-2776(08)60403-4.

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Strieter, R. M., and B. N. Gomperts. "CHEMOKINES, CXC | CXCL12 (SDF-1)." In Encyclopedia of Respiratory Medicine, 390–94. Elsevier, 2006. http://dx.doi.org/10.1016/b0-12-370879-6/00468-3.

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Conference papers on the topic "Chemokine SDF-1"

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Cain, James P., Christina A. Chantell, Michael A. Onaiyekan, and Mahendra Menakuru. "Fast Solid-Phase Peptide Synthesis of β-Amyloid (1-42) and the 68-mer Chemokine SDF-1α on the Symphony XTM Multiplex Peptide Synthesizer." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.220.

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Halimi, Caroline, Sébastien Albert, Annemilai Tijeras-Raballand, Lucile Astorgues-Xerri, Anne Couvelard, Muriel Hourseau, Maria Eugenia Riveiro, Maria Serova, Eric Raymond, and Sandrine J. Faivre. "Abstract 728: CXCL12 (SDF-1) chemokine expression as a baseline factor associated with resistance to induction chemotherapy in head and neck squamous cell carcinoma." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-728.

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Trubelja, Alen, John W. MacArthur, Joseph J. Sarver, Jeffrey E. Cohen, Yasuhiro Shudo, Alexander S. Fairman, Jay Patel, William Hiesinger, Pavan Atluri, and Y. Joseph Woo. "Bioengineered SDF-1a Analogue Delivered as an Angiogenic Therapy Significantly Normalizes Elastic and Viscoelastic Material Properties of Infarcted Cardiac Muscle." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14602.

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Heart disease is a leading cause of death worldwide, and coronary heart disease causes 1 of every 6 deaths in the United States [1]. Following a myocardial infarction, scar tissue gradually replaces myocardium that is lost through a process of collagen deposition and an increase in tensile strength of the tissue [2]. This leads to infarct expansion, adverse ventricular remodeling and dysfunction, and ultimately heart failure. Dilation of the left ventricle (LV) leads to increased LV wall stress and is ultimately responsible for adverse ventricular remodeling. LV dilation causes stretching and thereby increased wall stress, prohibiting cardiomyocytes from effectively contracting, which leads to further dilation, and ultimately a decrease in cardiac pump efficiency [3]. Previously, it has been shown that using a tissue filler to modify the material properties of an infarct limits the process of ventricular remodeling [4]. Angiogenesis is another mechanism by which adverse ventricular remodeling can be limited. Previously, our group developed engineered stromal cell-derived factor-1α (ESA), a computationally designed analog of an established endothelial progenitor cell chemokine, SDF-1α, and demonstrated that ESA injection enhances LV function by promoting angiogenesis and retains the native properties of the extracellular matrix (ECM) [5] [6]. In this study, we propose that injection of ESA to infarcted cardiac muscle improves the tensile strength and viscoelastic properties of ventricular muscle.
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Pavlasova, Gabriela, Marek Borsky, Vaclav Seda, Katerina Cerna, Jitka Osickova, Michael Doubek, Yvona Brychtova, et al. "Abstract 3291: The expression of CD20 on malignant B cells is regulated by chemokine signaling through the CXCR4/SDF-1 axis: implications for targeting the microenvironmental interactions." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3291.

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