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本文引用的文献

1
Ischemia-induced neural stem/progenitor cells in the pia mater following cortical infarction.皮质梗死灶下软脑膜内缺血诱导的神经干细胞/祖细胞。
Stem Cells Dev. 2011 Dec;20(12):2037-51. doi: 10.1089/scd.2011.0279. Epub 2011 Aug 12.
2
Immortalized CNS pericytes are quiescent smooth muscle actin-negative and pluripotent.永生化中枢神经系统周细胞静息,平滑肌肌动蛋白阴性,多能性。
Microvasc Res. 2011 Jul;82(1):18-27. doi: 10.1016/j.mvr.2011.04.003. Epub 2011 Apr 15.
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The Fowler syndrome-associated protein FLVCR2 is an importer of heme.Fowler 综合征相关蛋白 FLVCR2 是血红素的输入蛋白。
Mol Cell Biol. 2010 Nov;30(22):5318-24. doi: 10.1128/MCB.00690-10. Epub 2010 Sep 7.
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High-throughput sequencing of a 4.1 Mb linkage interval reveals FLVCR2 deletions and mutations in lethal cerebral vasculopathy.高通量测序 4.1Mb 连锁区间揭示致死性脑血管病中 FLVCR2 的缺失和突变。
Hum Mutat. 2010 Oct;31(10):1134-41. doi: 10.1002/humu.21329.
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Isolation of locally derived stem/progenitor cells from the peri-infarct area that do not migrate from the lateral ventricle after cortical stroke.从皮质卒中后不从侧脑室迁移的梗死周边区分离局部来源的干细胞/祖细胞。
Stroke. 2010 Sep;41(9):e552-60. doi: 10.1161/STROKEAHA.110.589010. Epub 2010 Jul 29.
6
Subventricular zone-derived neural progenitor cells migrate along a blood vessel scaffold toward the post-stroke striatum.室下区源性神经祖细胞沿着血管支架迁移到卒中后的纹状体。
Stem Cells. 2010 Mar 31;28(3):545-54. doi: 10.1002/stem.306.
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Inducing stroke in aged, hypertensive, diabetic rats.诱导老龄、高血压、糖尿病大鼠发生中风。
J Cereb Blood Flow Metab. 2010 Apr;30(4):729-33. doi: 10.1038/jcbfm.2009.273. Epub 2010 Jan 13.
8
Ischemia-induced neurogenesis of neocortical layer 1 progenitor cells.缺血诱导新皮层 1 层祖细胞的神经发生。
Nat Neurosci. 2010 Feb;13(2):173-9. doi: 10.1038/nn.2473. Epub 2009 Dec 27.
9
Pericyte contraction induced by oxidative-nitrative stress impairs capillary reflow despite successful opening of an occluded cerebral artery.尽管闭塞的脑动脉成功开通,但氧化-硝化应激诱导的周细胞收缩会损害毛细血管再灌注。
Nat Med. 2009 Sep;15(9):1031-7. doi: 10.1038/nm.2022. Epub 2009 Aug 30.
10
Isolation and characterization of neural stem/progenitor cells from post-stroke cerebral cortex in mice.从小鼠中风后大脑皮层分离并鉴定神经干/祖细胞
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一种新型的α-平滑肌肌动蛋白阳性细胞在大鼠中风模型中被激活:对其在缺血反应中的时空分布的分析。

A novel population of α-smooth muscle actin-positive cells activated in a rat model of stroke: an analysis of the spatio-temporal distribution in response to ischemia.

机构信息

Cardiology Department, Austin Health, Melbourne, Victoria, Australia.

出版信息

J Cereb Blood Flow Metab. 2012 Nov;32(11):2055-65. doi: 10.1038/jcbfm.2012.107. Epub 2012 Jul 18.

DOI:10.1038/jcbfm.2012.107
PMID:22805872
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3493995/
Abstract

In a rat model of stroke, the spatio-temporal distribution of α-smooth muscle actin-positive, (αSMA+) cells was investigated in the infarcted hemisphere (ipsilateral) and compared with the contralateral hemisphere. At day 3 postischemia, αSMA+ cells were concentrated in two main loci within the ipsilateral hemisphere (Area A) in the medial corpus callosum and (Area B) midway through the striatum adjacent to the lateral ventricle. By day 7 and further by day 14, fewer αSMA+ cells remained in Areas A and B but a steady increase in the peri-infarct was observed. αSMA+ cells also expressed glial acidic fibrillary protein [GFAP: αSMA+/GFAP+ (29%); αSMA+/GFAP- (71%) phenotypes] and feline leukemia virus C receptor 2 (FLVCR2), but not ED1(microglia) and established markers of pericytes normally located in vascular wall. αSMA+ cells were also located close to the subventricular zones (SVZ) adjacent to Areas A and B. In conclusion, αSMA+ cells have been identified in a spatial and temporal sequence from the SVZ, at intermediate loci and in the vicinity of the peri-infarct. It is hypothesized that novel populations of αSMA+ precursors of pericytes are born on the SVZ, migrate into the peri-infarct region and are incorporated into new vessels of the peri-infarct regions.

摘要

在中风大鼠模型中,研究了梗死侧(同侧)和对侧半球中α-平滑肌肌动蛋白阳性(αSMA+)细胞的时空分布。在缺血后 3 天,αSMA+细胞集中在同侧半球的两个主要部位(区域 A)在胼胝体的内侧和(区域 B)在靠近侧脑室的纹状体中部。到第 7 天和进一步到第 14 天,区域 A 和 B 中剩余的αSMA+细胞减少,但在梗死周围观察到稳定的增加。αSMA+细胞还表达神经胶质酸性纤维蛋白[GFAP:αSMA+/GFAP+(29%);αSMA+/GFAP-(71%)表型]和猫白血病病毒 C 受体 2(FLVCR2),但不表达 ED1(小胶质细胞)和通常位于血管壁的周细胞的标志性蛋白。αSMA+细胞也靠近与区域 A 和 B 相邻的侧脑室下区(SVZ)。总之,已经在 SVZ、中间部位和梗死周围区域以时空顺序鉴定出 αSMA+细胞。据推测,周细胞的新型αSMA+前体细胞是在 SVZ 产生的,迁移到梗死周围区域,并整合到梗死周围区域的新血管中。