Literature DB >> 8780792

Apoptosis in focal cerebral ischemia.

M Chopp1, Y Li.   

Abstract

An ischemic insult to the brain evokes cell damage which may progress to cell death. We invariably associated cell death with necrosis. Necrosis exhibits well defined morphological characteristics, and the biochemical and biophysical processes associated with necrosis have been identified. However, another form of cell death exists, apoptosis. Apoptosis plays an important role in the early development of tissues. Cells undergoing apoptosis exhibit very different morphological characteristics and temporal profiles of change from cells undergoing necrosis. Apoptosis has been identified with the internucleosomal fragmentation of DNA. More importantly, apoptosis has been associated with a process of programmed cell death, in which a genetic program is activated which results in the death of the cell. In this presentation, we will review our data on the morphological, biochemical and molecular evidence of apoptosis in the rodent (rat, mouse) brain after middle cerebral artery occlusion. Emphasis will be placed on describing the temporal profile and the anatomical distribution of cells undergoing apoptosis as functions of duration of MCA occlusion and reperfusion after MCA occlusion. This possible contribution of selective genes in promoting and/or inhibiting apoptosis will also be discussed.

Entities:  

Mesh:

Year:  1996        PMID: 8780792     DOI: 10.1007/978-3-7091-9465-2_4

Source DB:  PubMed          Journal:  Acta Neurochir Suppl        ISSN: 0065-1419


  18 in total

1.  Incorporation of sodium channel blocking and free radical scavenging activities into a single drug, AM-36, results in profound inhibition of neuronal apoptosis.

Authors:  J K Callaway; P M Beart; B Jarrott; S F Giardina
Journal:  Br J Pharmacol       Date:  2001-04       Impact factor: 8.739

Review 2.  Neuroprotective effect of an antioxidant in ischemic brain injury: involvement of neuronal apoptosis.

Authors:  Miki Fujimura; Teiji Tominaga; Pak H Chan
Journal:  Neurocrit Care       Date:  2005       Impact factor: 3.210

3.  Apoptosis has a prolonged role in the neurodegeneration after hypoxic ischemia in the newborn rat.

Authors:  W Nakajima; A Ishida; M S Lange; K L Gabrielson; M A Wilson; L J Martin; M E Blue; M V Johnston
Journal:  J Neurosci       Date:  2000-11-01       Impact factor: 6.167

4.  The role of HSPA12B in regulating neuronal apoptosis.

Authors:  Lihua Kang; Guowei Zhang; Yaohua Yan; Kaifu Ke; Xinmin Wu; Yilu Gao; Jing Li; Lin Zhu; Qiyun Wu; Zhengming Zhou
Journal:  Neurochem Res       Date:  2013-01-05       Impact factor: 3.996

5.  MicroRNA-21 protects neurons from ischemic death.

Authors:  Ben Buller; Xianshuang Liu; Xinli Wang; Rui L Zhang; Li Zhang; Ann Hozeska-Solgot; Michael Chopp; Zheng G Zhang
Journal:  FEBS J       Date:  2010-09-14       Impact factor: 5.542

6.  Mechanisms of cell death induced by the mitochondrial toxin 3-nitropropionic acid: acute excitotoxic necrosis and delayed apoptosis.

Authors:  Z Pang; J W Geddes
Journal:  J Neurosci       Date:  1997-05-01       Impact factor: 6.167

7.  Ionic mechanism of ouabain-induced concurrent apoptosis and necrosis in individual cultured cortical neurons.

Authors:  Ai Ying Xiao; Ling Wei; Shuli Xia; Steven Rothman; Shan Ping Yu
Journal:  J Neurosci       Date:  2002-02-15       Impact factor: 6.167

Review 8.  MicroRNAs regulate the chaperone network in cerebral ischemia.

Authors:  Yi-Bing Ouyang; Rona G Giffard
Journal:  Transl Stroke Res       Date:  2013-08-17       Impact factor: 6.829

Review 9.  Advances in astrocyte-targeted approaches for stroke therapy: an emerging role for mitochondria and microRNAS.

Authors:  Creed M Stary; Rona G Giffard
Journal:  Neurochem Res       Date:  2014-07-04       Impact factor: 3.996

Review 10.  microRNAs: innovative targets for cerebral ischemia and stroke.

Authors:  Yi-Bing Ouyang; Creed M Stary; Guo-Yuan Yang; Rona Giffard
Journal:  Curr Drug Targets       Date:  2013-01-01       Impact factor: 3.465

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.