کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8455204 | 1548011 | 2015 | 60 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Deletion of ADAMTS5 does not affect aggrecan or versican degradation but promotes glucose uptake and proteoglycan synthesis in murine adipose derived stromal cells
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
LRP1chondroitin/dermatan sulfateVCANVersicanACANAggrecanA2MADAMTS5ECMBMP7TGF-β1ADSCalpha-2-macroglobulin - آلفا 2-ماگروگلوبولینIHC - ایمونوهیستوشیمیImmunohistochemistry - ایمونوهیستوشیمیTransforming growth factor beta-1 - تبدیل فاکتور رشد بتا-1Degradation - تنزلAdipose derived stromal cells - سلول های استرومای مشتق شده از چربیMesenchymal stem cells - سلول های بنیادی مزانشیمیExtracellular matrix - ماتریکس خارج سلولیknockout - ناکاوتwild type - نوع وحشیHyaluronan - هیالورونانbone morphogenetic protein 7 - پروتئین مورفوژنیک استخوان 7
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
ADAMTS5 (TS5), a member of the aggrecanase clade (TS1, 4, 5, 8, 9, 15) of ADAMTS-proteases, has been considered largely responsible for the proteolysis of the hyalectans, aggrecan (Acan) and versican (Vcan), in vivo. However, we have reported that ts5-knockout (KO) mice show joint protection after injury due to inhibition of synovial scarring and enhanced Acan deposition. Also, KO mice have an impaired wound healing phenotype in skin and tendons which is associated with Acan/Vcan-rich deposits at the wound sites. Moreover, the Acan and Vcan deposited was aggrecanase-cleaved, even in the absence of TS5. In this study, we have used adipose-derived stromal cell (ADSC) and epiphyseal chondrocyte cultures from wild type and KO mice to further study the role of TS5 in Acan and Vcan turnover. We have confirmed with both cell types that the aggrecanase-mediated degradation of these hyalectans is not due to TS5, but an aggrecanase which primarily cleaves them before they are secreted. We also provide data which suggests that TS5 protein functions to suppress glucose uptake in ADSCs and thereby inhibits the synthesis, and promotes the intracellular degradation of Acan and Vcan by an ADAMTS other than TS5. We propose that this apparently non-proteolytic role of TS5 explains its anti-chondrogenic and pro-fibrotic effects in murine models of wound repair. A possible role for TS5 in an endocytotic process, involving competitive interactions between TS5, LRP1 and GLUT4 is discussed.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Matrix Biology - Volume 47, September 2015, Pages 66-84
Journal: Matrix Biology - Volume 47, September 2015, Pages 66-84
نویسندگان
Daniel J. Gorski, Wenfeng Xiao, Jun Li, Wei Luo, Mark Lauer, John Kisiday, Anna Plaas, John Sandy,