Tags

Type your tag names separated by a space and hit enter

Development of cerebral infarction, apoptotic cell death and expression of X-chromosome-linked inhibitor of apoptosis protein following focal cerebral ischemia in rats.
Life Sci. 2006 Jan 11; 78(7):704-12.LS

Abstract

The aim of this study was to investigate the role of apoptosis or necrosis in the development of delayed infarct, and the relationship between the level of XIAP gene, caspase-3 activation and ischemic cell death following transient focal cerebral ischemia. Adult male Sprague-Dawley rats underwent right middle cerebral artery occlusion (MCAo) for 50 min and reperfusion for 0.5, 4, 8, 24 h, 3, 7, 14 days. On TTC-stained coronal sections, delayed infarct was observed to develop in the whole MCA territory, especially in frontoparietal cortex after ischemia. Near total infarct was shown in striatum 24 h after MCAo, while delayed infarct was evident in the cortex. By day 3, the infarct had progressively expanded to the nearly whole area of the frontoparietal cortex. Flow cytometric analysis of Annexin-V (marks apoptosis) and PI (propidium iodide, marks necrosis) labeling cells showed that MCAo dominantly induced necrosis in ischemic core, striatum. Apoptosis contributed to delayed infarct and cell death in the border zone, dorsolateral cortex and hippocampus. The time-course of caspase-3 activation was consistent with the changes of apoptosis and infarct following MCAo. Further RT-PCR experiments indicated that there was a biphasic regulation of XIAP in time- and region-dependent manner after ischemia. In the infarct core (striatum), following a transient and slight increase during 0.5 h to 4 h post-MCAo, expression of XIAP mRNA markedly decreased. On the other hand, a longer and larger upregulation of XIAP was observed at early time points in border zone (0.5 to 8 h, in dorsolateral cortex; 0.5 to 24 h in hippocampus), then the level of XIAP reduced. A negative correlation was observed between apoptosis and regulation of XIAP gene in these regions. Our findings suggest a possible association between expression of XIAP gene, apoptosis and delayed infarct following ischemia.

Authors+Show Affiliations

Chemistry and Life Science College, Zhejiang Normal University, Jinhua, 321004, P.R. China. xuxh63@zjnu.cnNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16139848

Citation

Xu, Xiao-Hong, et al. "Development of Cerebral Infarction, Apoptotic Cell Death and Expression of X-chromosome-linked Inhibitor of Apoptosis Protein Following Focal Cerebral Ischemia in Rats." Life Sciences, vol. 78, no. 7, 2006, pp. 704-12.
Xu XH, Zhang SM, Yan WM, et al. Development of cerebral infarction, apoptotic cell death and expression of X-chromosome-linked inhibitor of apoptosis protein following focal cerebral ischemia in rats. Life Sci. 2006;78(7):704-12.
Xu, X. H., Zhang, S. M., Yan, W. M., Li, X. R., Zhang, H. Y., & Zheng, X. X. (2006). Development of cerebral infarction, apoptotic cell death and expression of X-chromosome-linked inhibitor of apoptosis protein following focal cerebral ischemia in rats. Life Sciences, 78(7), 704-12.
Xu XH, et al. Development of Cerebral Infarction, Apoptotic Cell Death and Expression of X-chromosome-linked Inhibitor of Apoptosis Protein Following Focal Cerebral Ischemia in Rats. Life Sci. 2006 Jan 11;78(7):704-12. PubMed PMID: 16139848.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Development of cerebral infarction, apoptotic cell death and expression of X-chromosome-linked inhibitor of apoptosis protein following focal cerebral ischemia in rats. AU - Xu,Xiao-Hong, AU - Zhang,Shao-Min, AU - Yan,Wei-Ming, AU - Li,Xiao-Rong, AU - Zhang,Heng-Yi, AU - Zheng,Xiao-Xiang, Y1 - 2005/09/01/ PY - 2004/09/24/received PY - 2005/05/10/accepted PY - 2005/9/6/pubmed PY - 2006/2/17/medline PY - 2005/9/6/entrez SP - 704 EP - 12 JF - Life sciences JO - Life Sci VL - 78 IS - 7 N2 - The aim of this study was to investigate the role of apoptosis or necrosis in the development of delayed infarct, and the relationship between the level of XIAP gene, caspase-3 activation and ischemic cell death following transient focal cerebral ischemia. Adult male Sprague-Dawley rats underwent right middle cerebral artery occlusion (MCAo) for 50 min and reperfusion for 0.5, 4, 8, 24 h, 3, 7, 14 days. On TTC-stained coronal sections, delayed infarct was observed to develop in the whole MCA territory, especially in frontoparietal cortex after ischemia. Near total infarct was shown in striatum 24 h after MCAo, while delayed infarct was evident in the cortex. By day 3, the infarct had progressively expanded to the nearly whole area of the frontoparietal cortex. Flow cytometric analysis of Annexin-V (marks apoptosis) and PI (propidium iodide, marks necrosis) labeling cells showed that MCAo dominantly induced necrosis in ischemic core, striatum. Apoptosis contributed to delayed infarct and cell death in the border zone, dorsolateral cortex and hippocampus. The time-course of caspase-3 activation was consistent with the changes of apoptosis and infarct following MCAo. Further RT-PCR experiments indicated that there was a biphasic regulation of XIAP in time- and region-dependent manner after ischemia. In the infarct core (striatum), following a transient and slight increase during 0.5 h to 4 h post-MCAo, expression of XIAP mRNA markedly decreased. On the other hand, a longer and larger upregulation of XIAP was observed at early time points in border zone (0.5 to 8 h, in dorsolateral cortex; 0.5 to 24 h in hippocampus), then the level of XIAP reduced. A negative correlation was observed between apoptosis and regulation of XIAP gene in these regions. Our findings suggest a possible association between expression of XIAP gene, apoptosis and delayed infarct following ischemia. SN - 0024-3205 UR - https://www.unboundmedicine.com/medline/citation/16139848/Development_of_cerebral_infarction_apoptotic_cell_death_and_expression_of_X_chromosome_linked_inhibitor_of_apoptosis_protein_following_focal_cerebral_ischemia_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(05)00700-9 DB - PRIME DP - Unbound Medicine ER -