Journal
ANIMAL CELLS AND SYSTEMS
Volume 26, Issue 1, Pages 10-18Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/19768354.2021.2023037
Keywords
Connexin proteins; gap junctions; HUVECs; mechanism; simvastatin
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Funding
- National Natural Science Foundation of China [81373960, 81573600]
- Science and Technology Planning Project of Guangdong Province, China [2014A020212416]
- Guangzhou Science and Technology Plan Project, China [201707010132]
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This study found that simvastatin regulates gap junction function in vascular endothelial cells by upregulating Cx37 and Cx40 expression and downregulating Cx43 expression.
Although simvastatin has been shown to inhibit vascular permeability, which might be amplified via gap junction intercellular communication (GJIC), the underlying mechanism of action remains unclear. In the present study, we investigated the effects and mechanisms of simvastatin on endothelial cells GJIC. Specifically, human umbilical vein endothelial cells (HUVECs) were stimulated with TNF-alpha (10 ng/mL) alone or in combination with simvastatin (5 mu M), and their effects on vascular endothelial cell GJIC tested via the scrape loading/dye transfer (SL/DT) assay. Next, we performed immunofluorescence, real-time PCR and western blot assays to analyze expression of Cx37, Cx40 and Cx43 in HUVECs. Results showed that GJIC activity in HUVECs was markedly elevated in HUVECs treated with TNF-alpha in combination with simvastatin. In addition, simvastatin treatment significantly upregulated expression of Cx37 and Cx40 but downregulated Cx43 mRNAs and proteins. Taken together, these marked changes indicated that simvastatin exerts its regulatory effects on gap junction function by upregulating Cx37 and Cx40 and downregulating Cx43 expression.
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