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The key target of neuroprotection after the onset of ischemic stroke: secretory pathway Ca(2+)-ATPase 1.

Li LH, Tian XR, Hu ZP - Neural Regen Res (2015)

Bottom Line: Levels of Golgi Ca(2+) showed an opposite effect.This variation was similar to the alteration of calcium in separated Golgi vesicles.The secretory pathway Ca(2+)-ATPase 1 can be an important neuroprotective target of ischemic stroke.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Jishou University, Jishou, Hunan Province, China ; Department of Neurology, Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.

ABSTRACT
The regulatory mechanisms of cytoplasmic Ca(2+) after myocardial infarction-induced Ca(2+) overload involve secretory pathway Ca(2+)-ATPase 1 and the Golgi apparatus and are well understood. However, the effect of Golgi apparatus on Ca(2+) 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 Ca(2+)-ATPase 1 in the cortex and hippocampus was detected by immunoblotting, and Ca(2+) concentrations in the cytoplasm and Golgi vesicles were determined. Results showed an overload of cytoplasmic Ca(2+) during ischemia and reperfusion that reached a peak after reperfusion. Levels of Golgi Ca(2+) showed an opposite effect. The expression of Golgi-specific secretory pathway Ca(2+)-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 Ca(2+)-ATPase 1 tightly responds to ischemia and reperfusion in nerve cells. Thus, we concluded that secretory pathway Ca(2+)-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 Ca(2+)-ATPase 1 can be an important neuroprotective target of ischemic stroke.

No MeSH data available.


Related in: MedlinePlus

Changes in Ca2+ concentration in cytoplasm and separated Golgi vesicles in nerve cells during cerebral ischemia and reperfusion.(A) Changes in cytoplasmic Ca2+, which increased rapidly during ischemia and early reperfusion and then slightly but appreciably declined. (B) Changes in Golgi Ca2+, which showed an opposite trend to cytoplasmic Ca2+. C: Control group; S: sham operation group; I: ischemia group; R: reperfusion group; h: hours; d: days. The data are expressed as the mean ± SEM (calculated from data of five pieces of brain section) and oneway analysis of variance followed by the least significance difference test was used.
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Figure 1: Changes in Ca2+ concentration in cytoplasm and separated Golgi vesicles in nerve cells during cerebral ischemia and reperfusion.(A) Changes in cytoplasmic Ca2+, which increased rapidly during ischemia and early reperfusion and then slightly but appreciably declined. (B) Changes in Golgi Ca2+, which showed an opposite trend to cytoplasmic Ca2+. C: Control group; S: sham operation group; I: ischemia group; R: reperfusion group; h: hours; d: days. The data are expressed as the mean ± SEM (calculated from data of five pieces of brain section) and oneway analysis of variance followed by the least significance difference test was used.

Mentions: Calcium detection in isolated nerve cells showed that cytoplasmic Ca2+ increased rapidly in ischemia and early reperfusion and then slightly but appreciably declined. After reperfusion of 3 hours, the Ca2+ labeled by Fura-2/AM was at its maximum value, 1,695.5 nM, which was eight times higher than the control (P = 0.001). Calcium overload was sustained and the concentration remained twice higher than the control (P = 0.003) until the time of reperfusion for 7 days. Although calcium overload remained to the time of reperfusion for 7 days, there was an obvious alleviation in late reperfusion (Figure 1A).


The key target of neuroprotection after the onset of ischemic stroke: secretory pathway Ca(2+)-ATPase 1.

Li LH, Tian XR, Hu ZP - Neural Regen Res (2015)

Changes in Ca2+ concentration in cytoplasm and separated Golgi vesicles in nerve cells during cerebral ischemia and reperfusion.(A) Changes in cytoplasmic Ca2+, which increased rapidly during ischemia and early reperfusion and then slightly but appreciably declined. (B) Changes in Golgi Ca2+, which showed an opposite trend to cytoplasmic Ca2+. C: Control group; S: sham operation group; I: ischemia group; R: reperfusion group; h: hours; d: days. The data are expressed as the mean ± SEM (calculated from data of five pieces of brain section) and oneway analysis of variance followed by the least significance difference test was used.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4590240&req=5

Figure 1: Changes in Ca2+ concentration in cytoplasm and separated Golgi vesicles in nerve cells during cerebral ischemia and reperfusion.(A) Changes in cytoplasmic Ca2+, which increased rapidly during ischemia and early reperfusion and then slightly but appreciably declined. (B) Changes in Golgi Ca2+, which showed an opposite trend to cytoplasmic Ca2+. C: Control group; S: sham operation group; I: ischemia group; R: reperfusion group; h: hours; d: days. The data are expressed as the mean ± SEM (calculated from data of five pieces of brain section) and oneway analysis of variance followed by the least significance difference test was used.
Mentions: Calcium detection in isolated nerve cells showed that cytoplasmic Ca2+ increased rapidly in ischemia and early reperfusion and then slightly but appreciably declined. After reperfusion of 3 hours, the Ca2+ labeled by Fura-2/AM was at its maximum value, 1,695.5 nM, which was eight times higher than the control (P = 0.001). Calcium overload was sustained and the concentration remained twice higher than the control (P = 0.003) until the time of reperfusion for 7 days. Although calcium overload remained to the time of reperfusion for 7 days, there was an obvious alleviation in late reperfusion (Figure 1A).

Bottom Line: Levels of Golgi Ca(2+) showed an opposite effect.This variation was similar to the alteration of calcium in separated Golgi vesicles.The secretory pathway Ca(2+)-ATPase 1 can be an important neuroprotective target of ischemic stroke.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Jishou University, Jishou, Hunan Province, China ; Department of Neurology, Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.

ABSTRACT
The regulatory mechanisms of cytoplasmic Ca(2+) after myocardial infarction-induced Ca(2+) overload involve secretory pathway Ca(2+)-ATPase 1 and the Golgi apparatus and are well understood. However, the effect of Golgi apparatus on Ca(2+) 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 Ca(2+)-ATPase 1 in the cortex and hippocampus was detected by immunoblotting, and Ca(2+) concentrations in the cytoplasm and Golgi vesicles were determined. Results showed an overload of cytoplasmic Ca(2+) during ischemia and reperfusion that reached a peak after reperfusion. Levels of Golgi Ca(2+) showed an opposite effect. The expression of Golgi-specific secretory pathway Ca(2+)-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 Ca(2+)-ATPase 1 tightly responds to ischemia and reperfusion in nerve cells. Thus, we concluded that secretory pathway Ca(2+)-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 Ca(2+)-ATPase 1 can be an important neuroprotective target of ischemic stroke.

No MeSH data available.


Related in: MedlinePlus