کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5509477 | 1400460 | 2016 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Coronin 1B serine 2 phosphorylation by p38α is critical for vascular endothelial growth factor-induced migration of human umbilical vein endothelial cells
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کلمات کلیدی
HUVECSS1PPDGFVSMCp38αArp2/3 - Arp2 / 3Sphingosine-1-phosphate - اسپینگسین-1-فسفاتVascular smooth muscle cell - سلول عضله صاف عروقیHuman umbilical vein endothelial cells - سلول های اندوتلیالی ورید ناف انسانVascular endothelial growth factor - فاکتور رشد اندوتلیال عروقیVascular Endothelial Growth Factor (VEGF) - فاکتور رشد اندوتلیال عروقی (VEGF)platelet-derived growth factor - فاکتور رشد حاصل از پلاکتMigration - مهاجرتactin-related protein 2/3 - پروتئین مرتبط با اکتین 2/3
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Coronin 1B is an actin-binding protein that regulates various cellular processes including cell motility. However, the role of coronin 1B in vascular cell migration remains controversial. Here, we examined the function of coronin 1B in vascular endothelial growth factor (VEGF)-induced migration of human umbilical vein endothelial cells (HUVECs) and investigated the mechanism by which coronin 1B regulates this cellular process. We found that depletion of coronin 1B increased the VEGF-induced migration of HUVECs. VEGF phosphorylated coronin 1B at Ser2 and stimulated its translocation to the leading edge of stimulated cells. Lentivirus-mediated overexpression of wild-type coronin 1B or a phosphodeficient coronin 1B S2A mutant decreased VEGF-induced transwell migration of HUVECs. Treatment with the p38 inhibitor SB203580 or depletion of p38α by small interfering RNA transfection decreased VEGF-induced coronin 1B phosphorylation. In vitro binding and kinase assays revealed that active p38α directly binds to and phosphorylates coronin 1B at Ser2. In addition, VEGF induced active p38α binding to coronin 1B in HUVECs. VEGF disrupted the interaction between coronin 1B and the actin-related protein (Arp)2/3 complex and p38α depletion prevented this VEGF-induced dissociation. These findings suggest that coronin 1B plays an inhibitory role in VEGF-induced migration of HUVECs and that VEGF-activated p38α phosphorylates coronin 1B at Ser2 and activates the Arp2/3 complex by liberating it from coronin 1B.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 28, Issue 12, December 2016, Pages 1817-1825
Journal: Cellular Signalling - Volume 28, Issue 12, December 2016, Pages 1817-1825
نویسندگان
Geun-Young Kim, Jin-Hee Park, Hanna Kim, Hyun-Joung Lim, Hyun-Young Park,