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Vascular endothelial growth factor/platelet-derived growth factor receptor pathway is involved in bone marrow mesenchymal stem cell differentiation and directional migration toward gliomas

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Neural Regeneration Research 2010年第13期5卷 993-998页

作者： Chaoshi Niu Yongfei Dong Ge Gao Department of Neurosurgery Anhui Provincial Hospital of Anhui Medical University Hefei 230001 Anhui Province China Molecular Neurobiology & Neural Regeneration and Repairing Laboratory Anhui Provincial Stereotactic Neurosurgical Institute Hefei 230001 Anhui Province China

BACKGROUND： Vascular endothelial growth factor （VEGF） induces bone marrow-derived mesenchymal stem cell （BMSC） differentiation into vascular endothelial-like cells and promotes BMSC migration toward gliomas. However, the molecular mechanisms by which VEGF induces BMSC differentiation and migration remain poorly understood. OBJECTIVE; To investigate the role of platelet-derived growth factor （PDGF） receptor （PDGFR） in BMSC differentiation and migration induced by VEGE DESIGN, TIME AND SETTING： A parallel, controlled, in vitro experiment was performed at the Molecular Neurobiology ＆ Neural Regeneration and Repairing Laboratory, Anhui Provincial Hospital of Anhui Medical University, China from June 2008 to March 2009. MATERIALS： U87 glioma cells were purchased from Shanghai Institutes for Biological Sciences; mouse anti-human PDGFR and VEGF receptor （VEGFR） monoclonal antibodies were purchased from Peprotech, USA. METHODS： Isolated BMSCs were precultured with neutralizing antibody for VEGFR-1, VEGFR-2, PDGFR-α, and PDGFR-β to block biological activity of related receptors, followed by induced differentiation with 50μg/L VEGF. BMSCs induced with 50μg/L VEGF alone served as the VEGF-induced group. The control group remained untreated. MAIN OUTCOME MEASURES： Cell surface markers were identified by flow cytometry; BMSC surface cytokine receptor expression was detected by reverse transcription-polymerase chain reaction; the Transwell model was used to observe cell migration. RESULTS： After blocking the PDGFR, VEGF did not induce BMSC cell surface marker CD-31 or von Willebrand factor （vWF） expression. However, inhibition with VEGF receptor blocking agents, VEGF induced BMSCs to express CD-31 and vWE Following inhibition of the PDGFR, the number of cells migrating through the polycarbonate membrane Transwell chamber was decreased, as well as the number of BMSCs migrating to glioma cells. However, through the use of VEGF receptor blocking agents, the number of migrating cells

关键词： vascular endothelial growth factor platelet-derived growth factor receptor bone marrow-derived mesenchymal stem cells glioma immunofluorescence

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PDGFR kinase inhibitor protects against septic death via regulation of BTLA

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Science China(Life Sciences) 2022年第10期65卷 1917-1928页

作者： Qiang Wang Jin Deng Jianhui Sun Huacai Zhang Di Liu Chu Gao Jinchao Qiu Wenyi Liu Guoxin Qu Dalin Wen Juan Du Anqiang Zhang Ling Zeng Jianxin Jiang Department of Trauma Medical Center Daping HospitalState Key Laboratory of TraumaBurns and Combined InjuryArmy Medical UniversityChongqing 400042China Department of Emergency the Affiliated Hospital of Guizhou Medical UniversityGuizhou Medical UniversityGuiyang 550001China

Sepsis,defined as life-threatening organ failure caused by a dysregulated host response to severe infection,is a major cause of death among intensive care unit *** targeting on immunomodulatory is a new research field in sepsis treatment.B-and T-lymphocyte attenuator(BTLA)is an inhibitory costimulatory factor molecule of B and T *** have shown that elevated expression of BTLA in lymphocytes can reduce mortality in sepsis,but its regulatory compounds and the underlying mechanism remains to be ***,we show that treatment with CP-673451 significantly decreases mortality of septic ***-673451 is a PDGFR kinase inhibitor which can promote the expression of BTLA,inhibit the release of chemokines such as CXCL13,and reduce first the chemotaxis of B cells to the peripheral blood and vital ***-673451 also inhibits both the release of cytokines and chemokines such as IL-1β,IL-6,IL-10,TNF-α,CCL1,CCL2 and CCL7 and reduces both the chemotactic ability of T *** suggests that CP-673451 may prevent septic death by inhibiting lymphocyte chemotaxis and alleviating“cytokine storm”.In conclusion,our study provides a new therapeutic target and an effective compound for sepsis treatment.

关键词： sepsis B-and T-lymphocyte attenuator platelet-derived growth factor receptor CP-673451 cytokine storm

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Multiple malignant extragastrointestinal stromal tumors of the greater omentum and results of immunohistochemistry and mutation analysis:A case report

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World Journal of Gastroenterology 2007年第24期13卷 3392-3395页

作者： Jong-Han Kim Yoon-Jung Boo Cheol-Woong Jung Sung-Soo Park Seung-Joo Kim Young-Jae Mok Sang-Dae Kim Yang-Suk Chae Chong-Suk Kim Kim Korea University Hospital Seoul 136-705 Korea Deparment of Surgery Pathology KoreaUniversity College of medicine Seoul 136-705 Korea

To report an extragastrointestinal stromal tumor （EGIST） that occurs outside the gastrointestinal tract and shows unique clinicopathologic and immunohistochemical features. In our case, we experienced multiple soft tissue tumors that originate primarily in the greater omentum, and in immunohistochemical analysis, the tumors showed features that correspond to malignant EGIST. Two large omental masses measured 15 cm×10 cm and 5 cm×4 cm sized and several small ovoid fragments were attached to small intestine, mesentery and peritoneum. On histologic findings, the masses were separated from small bowel serosa and had high mitotic count （115/50 HPFs）. In the results of immunohistochemical stains, the tumor showed CDl17 （c-kit） positive reactivity and high Ki-67 labeling index. On mutation analysis, the c-kit gene mutation was found in the juxtamembrane domain （exon 11）and it was heterozygote. platelet-derived growth factor receptor （PDGFR） gene mutation was also found in the juxtamemembrane （exon 12） and it was polymorphism. From above findings, we proposed that there may be several mutational pathways to malignant EGIST, so further investigations could be needed to approach this unfavorable disease entity.

关键词： Extragastrointestinal stromal tumor Greater omentum c-kit platelet-derived growth factor receptor Mutation

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Kawasaki Disease on PDGF Expression and VSMC Proliferation

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Journal of Huazhong University of Science and Technology(Medical Sciences) 1998年第4期18卷 243-246页

作者：王华王宏伟程佩萱 Department of Pediatrics Tongji Hospital Tongji Medical University Wuhan

The effect of serum of patients with Kawasaki disease (KD) on expression of platelet-derived growth factor (PDGF) B chain protein in vascular en-dothelial cells (VEC) was studied by immunocytochemical method. Meanwhile, the effects of the endothelial cell conditioned media (ECM) on expression of PDGF receptor mRNA in vascular smooth muscle cells (VSMC) and on cell cycle of VSMC were investigated by the methods of nucleic acid hybridization and flow cytometry (FCM). The results showed that the serum of patients with KD induced the expression of PDGF-B chain protein significantly. ECM significantly promoted the expression of PDGF receptor mRNA and induced the proliferation of VSMC. These data suggest that the activation of PDGF-PDGF receptor may play a role in the pathogenesis of coronary complication of KD.

关键词： Kawasaki disease platelet-derived growth factor platelet-derived growth factor receptor smooth muscle cell proliferation

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