缺血性中风
附带损害
神经外科
抵押品
神经学
医学
长非编码RNA
内科学
核糖核酸
神经科学
缺血
业务
生物
放射科
基因
心理学
遗传学
犯罪学
财务
作者
Anan Jiang,Zijie Wang,Ruey‐Kuang Cheng,Shaoru Zhang,Qisi Wu,Xinyue Qin
标识
DOI:10.1016/j.neurot.2024.e00429
摘要
Leptomeningeal anastomoses or pial collateral arteries are crucial for restoring cerebral blood flow (CBF) after an ischemic stroke. Vascular smooth muscle cells (VSMCs) are hypothesized to regulate the extent of this adaptive response, while the specific molecular mechanisms underlying this process are still being investigated. SNHG12, a long non-coding RNA, has been shown to influence several diseases related angiogenesis, including osteosarcoma and gastric cancer. However, the role of SNHG12 in contractile VSMC dedifferentiation during collateral arteriogenesis-related strokes remains unclear. Here we demonstrated that SNHG12 is a positive regulator of MMP9 and VSMC dedifferentiation, which enhances pial collateral arteriogenesis following cerebrovascular occlusion. Pial collateral remodeling is limited by the crosstalk between SNHG12-MMP9 signaling in VSMCs, which is mediated through repulsive guidance molecule a (RGMa) regulation. Thus, targeting SNHG12 may represent a therapeutic strategy for improving collateral function, neural tissue health, and functional recovery following ischemic stroke.
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