Changes in secretory pathway Ca(2+)-ATPase 2 following focal cerebral ischemia/reperfusion injury

Tonglin Lu; Zhiping Hu; Liuwang Zeng; Zheng Jiang

doi:10.3969/j.issn.1673-5374.2013.01.010

Changes in secretory pathway Ca(2+)-ATPase 2 following focal cerebral ischemia/reperfusion injury

Neural Regen Res. 2013 Jan 5;8(1):76-82. doi: 10.3969/j.issn.1673-5374.2013.01.010.

Authors

Tonglin Lu¹, Zhiping Hu¹, Liuwang Zeng¹, Zheng Jiang¹

Affiliation

¹ Department of Neurology, Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, China.

PMID: 25206375
PMCID: PMC4107497
DOI: 10.3969/j.issn.1673-5374.2013.01.010

Abstract

This study aimed to investigate changes in secretory pathway Ca(2+)-ATPase 2 expression following cerebral ischemia/reperfusion injury, and to define the role of Ca(2+)-ATPases in oxidative stress. A rat model of cerebral ischemia/reperfusion injury was established using the unilateral middle cerebral artery occlusion method. Immunohistochemistry and reverse transcription-PCR assay results showed that compared with the control group, the expression of secretory pathway Ca(2+)-ATPase 2 protein and mRNA in the cerebral cortex and hippocampus of male rats did not significantly change during the ischemic period. However, secretory pathway Ca(2+)-ATPase 2 protein and mRNA expression reduced gradually at 1, 3, and 24 hours during the reperfusion period. Our experimental findings indicate that levels of secretory pathway Ca(2+)-ATPase 2 protein and mRNA expression in brain tissue change in response to cerebral ischemia/reperfusion injury.

Keywords: Ca2+ oscillations; Ca2+-ATPase; Golgi apparatus; brain injury; cerebral infarction; focal cerebral ischemia; grants-supported paper; manganese; neural regeneration; neuroregeneration; oxidative damage; photographs-containing paper; secretory pathway Ca2+-ATPase 2.