作者: CHENG-HUNG CHEN , RICHARD S. BEARD , SHAWN E. BEARDEN
DOI: 10.1111/J.1549-8719.2012.00159.X
关键词: Immunology 、 Angiogenesis 、 Small hairpin RNA 、 Pharmacology 、 Protein kinase C 、 Wound healing 、 Biology 、 Cell growth 、 Agonist 、 Homocysteine 、 Metabotropic glutamate receptor 5
摘要: Please cite this paper as: Chen C-H, Beard RS, Bearden SE. Homocysteine impairs endothelial wound healing by activating metabotropic glutamate receptor 5. Microcirculation 19: 285–295, 2012. Abstract Objective: Hcy is an independent risk factor for cerebrovascular disease and cognitive impairment. The purpose of study was to elucidate the role mGluR5 in Hcy-mediated impairment cerebral repair. Methods: Mouse CMVECs (bEnd.3) were used conjunction with directed pharmacology shRNA. AutoDock simulate docking ligand–receptor interactions. Results: (20 μM) significantly increased Cx43-pS368 mGluR5- PKC-dependent mechanisms. attenuated repair mGluR5-dependent mechanism over six-day period but did not alter cell proliferation a assay, suggesting that attenuation may be due dysfunctional migration HHcy. expression Cx43 at edge mGluR5. Direct activation mGluR5, using specific agonist CHPG, sufficient reproduce results whereas KO shRNA, or inhibition MPEP, blocked response Hcy. Conclusions: Inhibition could novel strategy promoting patients Activation viable disrupting angiogenesis.