کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10144142 | 1646296 | 2018 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
SNHG12 Promotes Angiogenesis Following Ischemic Stroke via Regulating miR-150/VEGF Pathway
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کلمات کلیدی
BMECsFBSmiRNAslncRNAsOGDMCAOIBZlong noncoding RNAs - RNA های غیر Coding طولانیAngiogenesis - آنژیوژنزmiddle cerebral artery occlusion - انسداد شریان (سرخرگ) مغزی میانیRNA immunoprecipitation - ایمن سازی RNAmiR-150 - به miR-150microRNAs - ریز آرانایfetal bovine serum - سرم جنین گاوbrain microvascular endothelial cells - سلولهای اندوتلیالی مغز استخوان مغزIschemic stroke - سکته مغزی ایسکمیکVascular Endothelial Growth Factor (VEGF) - فاکتور رشد اندوتلیال عروقی (VEGF)Oxygen-glucose deprivation - محرومیت گلوکز اکسیژنRIP - پاره کردنoptical density - چگالی نوری
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The promotion of angiogenesis is a promising therapeutic strategy for ischemic stroke. Many long noncoding RNAs (lncRNAs) are related to angiogenesis following ischemic stroke. LncRNA small nucleolar RNA host gene 12 (SNHG12) was upregulated in oxygen-glucose deprivation (OGD)-exposed primary brain microvascular endothelial cells and in microvessel from middle cerebral artery occlusion (MCAO) animal brains. However, the role and underlying mechanism of SNHG12 in ischemic stroke especially associated with angiogenesis process remain unknown. The expression of SNHG12 and miR-150 was determined in OGD-stimulated mouse brain microvascular endothelial (bEnd.3) cells. The role and mechanism of SNHG12 in the angiogenesis after ischemic stroke were investigated using gain- and loss-of function approaches both in OGD-exposed bEnd.3 cells and in MCAO mouse models. We found SNHG12 expression was elevated, whereas miR-150 reduced in OGD-exposed bEnd.3 cells. Upregulation of SNHG12 elevated, and SNHG12 knockdown suppressed the capillary-like tube formation, viability, migration, and VEGF expression in OGD-injured bEnd.3 cells. miR-150 mimic reversed, whereas anti-miR-150 further strengthened the effect of SNHG12 upregulation on the angiogenesis in bEnd.3 cells. Furthermore, we found that SNHG12 functioned as a competing endogenous RNA for miR-150 to regulate VEGF expression. Additionally, overexpression of SNHG12 improved the recovery of neurological function, reduced infarct volume and miR-150 expression, increased vascular density and VEGF expression in the infarct border zone of MCAO mice. In conclusion, SNHG12 promotes the angiogenesis following ischemic stroke via miR-150/VEGF pathway, which further clarified the mechanism of angiogenesis after ischemic stroke and provides a target for the treatment of this disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 390, 15 October 2018, Pages 231-240
Journal: Neuroscience - Volume 390, 15 October 2018, Pages 231-240
نویسندگان
Mian Zhao, Jun Wang, Xinlong Xi, Nan Tan, Li Zhang,