4.5 Article

Spatial-temporal expression of NDRG2 in rat brain after focal cerebral ischemia and reperfusion

期刊

BRAIN RESEARCH
卷 1382, 期 -, 页码 252-258

出版社

ELSEVIER
DOI: 10.1016/j.brainres.2011.01.023

关键词

NDRG2; Focal cerebral ischemia; Astrocyte; Apoptosis

资金

  1. National Natural Science Foundation of China [30725039, 30930091, 30873326, 81072888, 81000563, 30600314, 30830054]
  2. National Key Basic Research and Development Program [2010CB529705]

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N-myc downstream regulated gene 2 (NDRG2) was reported to be widely expressed in the nervous system. However, the expression and potential role of NDRG2 in focal cerebral ischemia brain remain unclear. Herein, we investigated spatial-temporal expression of NDRG2 in the rat brain following transient focal cerebral ischemia. Male Sprague-Dawley rats underwent a 120-min transient occlusion of middle cerebral artery. Rats were killed and brain samples were harvested at 4, 12, 24, and 72 h after reperfusion. Expression of NDRG2 in the brain was determined by reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot analysis and immunohistochemical staining. Cellular apoptosis was assessed by TUNEL staining. The results showed that NDRG2 was expressed on cells with an astrocytes-like morphology in ischemic penumbra. NDRG2 mRNA and protein expression began to increase at 4 h after reperfusion and peaked at 24 h in the ischemic penumbra. By using immunofluorescence, NDRG2 signals were co-localized with GFAP-positive astrocytes, and NDRG2 expression in astrocytes translocated from a cytoplasm to a nuclear localization at 24 h after reperfusion. Double immunofiuorescent staining for TUNEL and NDRG2 showed that some NDRG2 signals co-localized with TUNEL-positive cells, and that the apoptotic cells increased with enhancement of NDRG2-positive signals. In conclusion, NDRG2 expression is up-regulated in ischemic penumbra following transient focal cerebral ischemia. NDRG2 expression in astrocytes may play important pathological roles in cell apoptosis after stroke. (C) 2011 Elsevier B.V. All rights reserved.

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