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10.1161/ATVBAHA.116.308895 http://scihub22266oqcxt.onion/10.1161/ATVBAHA.116.308895 C5503700!5503700!28473442     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Arterioscler+Thromb+Vasc+Biol 2017 ; 37 (7): 1352-60 Nephropedia Template TP {{tp|p=28473442|t=2017. Janus Kinase 3, a Novel Regulator for Smooth Muscle Proliferation and Vascular Remodeling |pdf=|usr=}}{{28473442}} gab.com Text Janus Kinase 3, a Novel Regulator for Smooth Muscle Proliferation and Vascular Remodeling JO: Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=28473442 #FOAvip Objective: Vascular remodeling due to smooth muscle cell (SMC) proliferation is a common process occurring in a number of vascular diseases such as atherosclerosis, aortic aneurysm, post-transplant vasculopathy, and restenosis after angioplasty, etc. The molecular mechanism underlying SMC proliferation, however, is not completed understood. The objective of this study is to determine the role and mechanism of Janus kinase 3 (JAK3) in vascular remodeling and SMC proliferation. Approach and Results: Platelet-derived growth factor (PDGF)-BB, a SMC mitogen, induces JAK3 expression and phosphorylation while stimulating SMC proliferation. Janex-1, a specific inhibitor of JAK3, or knockdown of JAK3 by shRNA, inhibits the SMC proliferation. Conversely, ectopic expression of JAK3 promotes SMC proliferation. Mechanistically, JAK3 promotes the phosphorylation of signal transducer and activator of transcription 3 and c-Jun N-terminal kinase in SMC, two signaling pathways known to be critical for SMC proliferation and vascular remodeling. Blockade of these two signaling pathways by their inhibitors impeded the JAK3-mediated SMC proliferation. In vivo, knockdown of JAK3 attenuates injury-induced neointima formation with attenuated neointimal SMC proliferation. Knockdown of JAK3 also induces neointimal SMC apoptosis in rat carotid artery balloon-injury model. Conclusion: Our results demonstrate that JAK3 mediates SMC proliferation and survival during injury-induced vascular remodeling, which provides a potential therapeutic target for preventing neointimal hyperplasia in proliferative vascular diseases. Twit Text FOAVip Janus Kinase 3, a Novel Regulator for Smooth Muscle Proliferation and Vascular Remodeling ????Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=28473442 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28473442 #FOAvip English Wikipedia <ref>{{Cite pmid|28473442}}</ref> Janus Kinase 3, a Novel Regulator for Smooth Muscle Proliferation and Vascular Remodeling #MMPMID28473442 Wang YC; Cui XB; Chuang YH; Chen SY Arterioscler Thromb Vasc Biol 2017[Jul]; 37 (7): 1352-60 PMID28473442show ga Objective: Vascular remodeling due to smooth muscle cell (SMC) proliferation is a common process occurring in a number of vascular diseases such as atherosclerosis, aortic aneurysm, post-transplant vasculopathy, and restenosis after angioplasty, etc. The molecular mechanism underlying SMC proliferation, however, is not completed understood. The objective of this study is to determine the role and mechanism of Janus kinase 3 (JAK3) in vascular remodeling and SMC proliferation. Approach and Results: Platelet-derived growth factor (PDGF)-BB, a SMC mitogen, induces JAK3 expression and phosphorylation while stimulating SMC proliferation. Janex-1, a specific inhibitor of JAK3, or knockdown of JAK3 by shRNA, inhibits the SMC proliferation. Conversely, ectopic expression of JAK3 promotes SMC proliferation. Mechanistically, JAK3 promotes the phosphorylation of signal transducer and activator of transcription 3 and c-Jun N-terminal kinase in SMC, two signaling pathways known to be critical for SMC proliferation and vascular remodeling. Blockade of these two signaling pathways by their inhibitors impeded the JAK3-mediated SMC proliferation. In vivo, knockdown of JAK3 attenuates injury-induced neointima formation with attenuated neointimal SMC proliferation. Knockdown of JAK3 also induces neointimal SMC apoptosis in rat carotid artery balloon-injury model. Conclusion: Our results demonstrate that JAK3 mediates SMC proliferation and survival during injury-induced vascular remodeling, which provides a potential therapeutic target for preventing neointimal hyperplasia in proliferative vascular diseases. äJanus Kinase 3, a Novel Regulator for Smooth Muscle Proliferation and (epmc).pdf DeepDyve Pubget Overpricing