The key target of neuroprotection after the onset of ischemic stroke： secretory pathway Ca2＋-ATPase 1

• Published in: Neural regeneration research Vol. 10; no. 8; pp. 1271 - 1278
• Main Authors: Li, Li-hua, Tian, Xiang-rong, Hu, Zhi-ping
• Format: Journal Article
• Language: English
• Published: India School of Medicine, Jishou University, Jishou, Hunan Province, China%Department of Neurology, Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China 01.08.2015; Medknow Publications & Media Pvt Ltd
• Subjects: ATP酶; Ca2; 分泌途径; 发病; 心肌梗死; 神经保护; 脑缺血再灌注; 高尔基体; Golgi Ca2; Golgi stress; Golgi apparatus; neural protection; homeostasis; brain injury; global cerebral ischemia; neural regeneration; cytoplasmic Ca2; nerve regeneration; secretory pathway Ca2+-ATPase 1; Ca2+ pump; NSFC grant
• ISSN: 1673-5374; 1876-7958
• DOI: 10.4103/1673-5374.162760

The regulatory mechanisms of cytoplasmic Ca2＋ after myocardial infarction-induced Ca2＋ overload involve secretory pathway Ca2＋-ATPase 1 and the Golgi apparatus and are well understood. However, the effect of Golgi apparatus on Ca2＋ overload after cerebral ischemia and reperfusion remains unclear. Four-vessel occlusion rats were used as animal models of cerebral ischemia. The expression of secretory pathway Ca2＋-ATPase 1 in the cortex and hippocampus was detected by immunoblotting, and Ca2＋ concentrations in the cytoplasm and Golgi vesicles were determined. Results showed an overload of cytoplasmic Ca2＋ during ischemia and reperfusion that reached a peak after reperfusion. Levels of Golgi Ca2＋ showed an opposite effect. The expression of Golgi-specific secretory pathway Ca2＋-ATPase 1 in the cortex and hippocampus decreased before ischemia and reperfusion, and increased after reperfusion for 6 hours. This variation was similar to the alteration of calcium in separated Golgi vesicles. These results indicate that the Golgi apparatus participates in the formation and alleviation of calcium overload, and that secretory pathway Ca2＋-ATPase 1 tightly responds to ischemia and reperfusion in nerve cells. Thus, we concluded that secretory pathway Ca2＋-ATPase 1 plays an essential role in cytosolic calcium regulation and its expression can be used as a marker of Golgi stress, responding to cerebral ischemia and reperfusion. The secretory pathway Ca2＋-ATPase 1 can be an important neuroprotective target of ischemic stroke.