Korean J Physiol Pharmacol.
2019 Mar;23(2):95-102. 10.4196/kjpp.2019.23.2.95.
Involvement of Orai1 in tunicamycin-induced endothelial dysfunction
- Affiliations
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- 1Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangzhou, Guangdong 510080, China. chunyudeng@126.com, raofang@medmail.com.cn
- 2Research Center of Medical Sciences, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, China.
- 3Department of Anesthesiology, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong 510623, China.
- 4Department of Pharmacy, Guangzhou Panyu Shiqiao Hospital, Guangzhou, Guangdong 511400, China.
- KMID: 2438083
- DOI: http://doi.org/10.4196/kjpp.2019.23.2.95
Abstract
- Endoplasmic reticulum (ER) stress is mediated by disturbance of Ca²âº homeostasis. The store-operated calcium (SOC) channel is the primary Ca²âº channel in non-excitable cells, but its participation in agent-induced ER stress is not clear. In this study, the effects of tunicamycin on Ca²âº influx in human umbilical vein endothelial cells (HUVECs) were observed with the fluorescent probe Fluo-4 AM. The effect of tunicamycin on the expression of the unfolded protein response (UPR)-related proteins BiP and CHOP was assayed by western blotting with or without inhibition of Orai1. Tunicamycin induced endothelial dysfunction by activating ER stress. Orai1 expression and the influx of extracellular Ca²âº in HUVECs were both upregulated during ER stress. The SOC channel inhibitor SKF96365 reversed tunicamycin-induced endothelial cell dysfunction by inhibiting ER stress. Regulation of tunicamycin-induced ER stress by Orai1 indicates that modification of Orai1 activity may have therapeutic value for conditions with ER stress-induced endothelial dysfunction.
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