Downregulated caveolin‑1 expression serves a potential role in coronary artery spasm by inducing nitric oxide production in vitro Corrigendum in /10.3892/etm.2024.12535

Cao,Xingmei; Ye,Zhishuai; Jin,Mingyu; Yan,Shuai; Song,Xiantao; Huang,Rongchong

doi:10.3892/etm.2018.6646

Downregulated caveolin‑1 expression serves a potential role in coronary artery spasm by inducing nitric oxide production in vitro

Corrigendum in: /10.3892/etm.2024.12535

Authors:
- Xingmei Cao
- Zhishuai Ye
- Mingyu Jin
- Shuai Yan
- Xiantao Song
- Rongchong Huang
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Affiliations: Department of Cardiology, Beijing An Zhen Hospital, Capital Medical University, Beijing 100029, P.R. China, Department of Cardiology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, P.R. China
Published online on: August 22, 2018 https://doi.org/10.3892/etm.2018.6646
Pages: 3567-3573
Copyright: © Cao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study aimed to investigate the effects of downregulated caveolin‑1 (Cav‑1) expression on nitric oxide (NO) production in lipopolysaccharide (LPS)‑damaged primary human umbilical vein endothelial cells (HUVECs) in a model of coronary artery spasm (CAS) microenvironment induced by acetylcholine (ACh) treatment. Small interfering RNA (siRNA)‑mediated Cav‑1 downregulation in HUVECs was confirmed by western blotting. The cell viability and superoxide dismutase (SOD) inhibition in HUVECs incubated with LPS (0, 10, 25, 50, 75 and 100 µg/ml) were measured by cell counting kit‑8 assay and a SOD kit, respectively. Intracellular Ca2+ [(Ca2+)i] in Fluo4‑acetoxymethyl ester‑loaded cells was detected by fluorescence microscopy. NO levels in the cell culture supernatants were measured by the nitrate reductase method. The results indicated that transfection with Cav‑1 siRNA, in particular siCav‑1 (2), downregulated the Cav‑1 protein expression. LPS at a dose of 75 µg/ml induced a significant decrease in HUVECs/si‑NC and HUVECs/siCav‑1 viability compared with the other concentrations of LPS. Compared with the effects of untreated cells, SOD inhibition in HUVECs/si‑NC and HUVECs/siCav‑1 was significantly decreased by LPS (75 µg/ml). In addition, ACh stimulation caused a greater increase in [Ca2+]i in HUVECs/si‑NC as compared with LPS‑treated HUVECs/si‑NC. ACh stimulation also induced significantly higher NO levels in LPS‑treated HUVECs/siCav‑1 compared with LPS‑treated HUVECs/si‑NC cells (P<0.05). In conclusion, the downregulated Cav‑1 expression served a key role in NO production in the in vitro model of CAS induced by ACh stimulation of LPS‑damaged HUVECs.

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