國家衛生研究院 NHRI:Item 3990099045/6599

NHRI > Institute of Biomedical Engineering and Nanomedicine > Jeng-Jiann Chiu > Periodical Articles > Item 3990099045/6599

Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/6599

Title:	Convergence of physical and chemical signaling in the modulation of vascular smooth muscle cell cycle and proliferation by fibrillar collagen-regulated P66Shc
Authors:	Yeh, YT;Lee, CI;Lim, SH;Chen, LJ;Wang, WL;Chuang, YJ;Chiu, JJ
Contributors:	Division of Medical Engineering Research
Abstract:	Arterial smooth muscle cell (SMC) phenotype and proliferation is regulated by their surrounding collagens, which transform from fibrillar to monomeric type in atherogenesis, and platelet-derived growth factor (PDGF)-BB/interleukin (IL)-1beta. This study aims at elucidating the mechanisms by which physical (monomeric vs. fibrillar collagens) and chemical (PDGF-BB/IL-1betavs. vehicle controls) stimuli modulate SMC cycle and proliferation. SMCs were cultured on monomeric vs. fibrillar type I collagens. In parallel experiments, SMCs on fibrillar collagen were co-stimulated with PDGF-BB/IL-1beta. These physical and chemical factors induced common SMC cycle signaling events, including up-regulations of cyclin-dependent kinase-4/6 and cyclins A/D1, phosphorylation of retinoblastoma (Rb) and its dissociations with E2F2/3. The physical and chemical inductions of SMC cycle signaling and progression were oppositely regulated by phosphatidylinositol 3-kinase (PI3K)-mediated Akt and p38 mitogen-activated protein kinase (MAPK). Fibrillar collagen degraded p66Shc, whose Ser36-phosphorylation plays important roles in the modulation of SMC cycle. Monomeric collagen and PDGF-BB/IL-1beta co-stimulation induced p66Shc expression and Ser36-phosphorylation through beta(1) integrin and PDGF receptor-beta, respectively. In conclusion, our results demonstrate that fibrillar collagen-regulated p66Shc converges the physical and chemical stimuli to modulate SMC cycle and proliferation through PI3K-mediated Akt and p38 MAPK and their opposite regulation in downstream common cell cycle signaling cascades.
Date:	2012-10
Relation:	Biomaterials. 2012 Oct;33(28):6728-6738.
Link to:	http://dx.doi.org/10.1016/j.biomaterials.2012.06.030
JIF/Ranking 2023:	http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0142-9612&DestApp=IC2JCR
Cited Times(WOS):	https://www.webofscience.com/wos/woscc/full-record/WOS:000308270000015
Cited Times(Scopus):	https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84864024239
Appears in Collections:	[Jeng-Jiann Chiu] Periodical Articles

Files in This Item:

File	Description	Size	Format
PUB2012072610.pdf		943Kb	Adobe PDF	693	View/Open

Loading...