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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

Broad expression of SPCA1 in the brain (immunofluorescence, fluorescence microscope).(A) Image of specimen without SPCA1 antibody, used as a reference. No fluorescent signals are detected. (B, C) SPCA1 expression in the brain, particularly in the cortex and hippocampus neurons, at 6 hours after reperfusion. SPCA1-immunoreactive cells show blue fluorescence. SPCA1: Secretory pathway Ca2+ ATPase 1.
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Figure 3: Broad expression of SPCA1 in the brain (immunofluorescence, fluorescence microscope).(A) Image of specimen without SPCA1 antibody, used as a reference. No fluorescent signals are detected. (B, C) SPCA1 expression in the brain, particularly in the cortex and hippocampus neurons, at 6 hours after reperfusion. SPCA1-immunoreactive cells show blue fluorescence. SPCA1: Secretory pathway Ca2+ ATPase 1.

Mentions: Direct fluorescence in situ detection of SPCA1 demonstrated that SPCA1 was widely expressed in cerebral tissues including cortex and hippocampus neurons (Figure 3) and showed an obvious change in response to ischemia and reperfusion (Figure 4A–H). When ischemia and early reperfusion occurred, the fluorescent density of SPCA1 primary antibodies was much weaker than the control, in particular, the density was at its lowest point during reperfusion (Figure 4C and D). After cerebral ischemia had ended, at reperfusion for approximately 6 hours, the fluorescent density increased to almost 200% of the control (P < 0.01; Figures 2 and 4E). Although the level of fluorescent density increased rapidly, it recovered to the normal level slowly (Figure 4F–H).


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)

Broad expression of SPCA1 in the brain (immunofluorescence, fluorescence microscope).(A) Image of specimen without SPCA1 antibody, used as a reference. No fluorescent signals are detected. (B, C) SPCA1 expression in the brain, particularly in the cortex and hippocampus neurons, at 6 hours after reperfusion. SPCA1-immunoreactive cells show blue fluorescence. SPCA1: Secretory pathway Ca2+ ATPase 1.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: Broad expression of SPCA1 in the brain (immunofluorescence, fluorescence microscope).(A) Image of specimen without SPCA1 antibody, used as a reference. No fluorescent signals are detected. (B, C) SPCA1 expression in the brain, particularly in the cortex and hippocampus neurons, at 6 hours after reperfusion. SPCA1-immunoreactive cells show blue fluorescence. SPCA1: Secretory pathway Ca2+ ATPase 1.
Mentions: Direct fluorescence in situ detection of SPCA1 demonstrated that SPCA1 was widely expressed in cerebral tissues including cortex and hippocampus neurons (Figure 3) and showed an obvious change in response to ischemia and reperfusion (Figure 4A–H). When ischemia and early reperfusion occurred, the fluorescent density of SPCA1 primary antibodies was much weaker than the control, in particular, the density was at its lowest point during reperfusion (Figure 4C and D). After cerebral ischemia had ended, at reperfusion for approximately 6 hours, the fluorescent density increased to almost 200% of the control (P < 0.01; Figures 2 and 4E). Although the level of fluorescent density increased rapidly, it recovered to the normal level slowly (Figure 4F–H).

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