Melatonin protected cardiac microvascular endothelial cells against oxidative stress injury via suppression of IP3R-[Ca 2+ ]c/VDAC-[Ca 2+ ]m axis by activation of MAPK/ERK signaling pathway
作者： Hang Zhu , Qinhua Jin , Yang Li , Qiang Ma , Jing Wang
DOI: 10.1007/S12192-017-0827-4
关键词:
摘要: The cardiac microvascular reperfusion injury is characterized by the endothelial cells (CMECs) oxidative damage which responsible for progression of dysfunction. However, few strategies are available to reverse such pathologies. This study aimed explore mechanism stress induced CMECs death and beneficial actions melatonin on survival, with a special focused IP3R-[Ca2+]c/VDAC-[Ca2+]m axis MAPK/ERK survival signaling. We found that H2O2 significantly activated cAMP response element binding protein (CREB) enhanced IP3R VDAC transcription expression, leading [Ca2+]c [Ca2+]m overload. High concentration suppressed ΔΨm, opened mPTP, released cyt-c into cytoplasm where it mitochondria-dependent pathway. could protect against via stimulation inactivated CREB therefore blocked IP3R/VDAC upregulation [Ca2+]c/[Ca2+]m overload, sustaining mitochondrial structural function integrity ultimately blockading mitochondrial-mediated cellular death. In summary, these findings confirmed mechanisms mitochondrial-involved provided an attractive effective way enhance survival.
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