Effect of endoplasmic reticulum stress in VEGF-induced neuroprotection.
Researchers suggest that endoplasmic reticulum (ER) stress cause apoptosis after ischemia. Caspase-12 has been localized to the ER and is a signal for apoptosis. We sought to clarify the role of caspase-12 in the vascular endothelial growth factor (VEGF) induced neuroprotective effect. Transient focal cerebral ischemia was produced by occluding left middle cerebral artery in rabbit. The expressions of caspase-12 and caspase-3 were detected by immunohistochemistry. Neuronal apoptosis was detected by TUNEL staining. We confirmed that the number of apoptotic cells and the expressions of caspase-12 and caspase-3 significantly increased during reperfusion. VEGF inhibited the cell apoptosis and the expressions of caspase-12 and caspase-3. These results suggest that VEGF may protect neurons from apoptosis by inhibiting ER stress pathway.
Yang
Ji-Ping
JP
Department of Medical Imaging, Second Hospital, Hebei Medical University, Shijiazhuang, Hebei Province, China.
Liu
Huai-Jun
HJ
Li
Ying
Y
D000818:Animals; D017209:Apoptosis; D053454:Caspase 12 / Q000378:metabolism*; D053148:Caspase 3 / Q000378:metabolism; D054022:Cerebrum / Q000473:pathology; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D005434:Flow Cytometry; D020287:In Situ Nick-End Labeling; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism* / Q000473:pathology; D008297:Male; D011817:Rabbits; D015424:Reperfusion; D015427:Reperfusion Injury / Q000473:pathology; D013312:Stress, Physiological; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
D042461:Vascular Endothelial Growth Factor A; D053454:Caspase 12; D053148:Caspase 3