The stimulatory effects of eNOS/F92A-Cav1 on NO production and angiogenesis in BMSCs

Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie
Peng XiaLexin Wang

Abstract

Nitric oxide (NO) is generated in endothelial cells by endothelial nitric oxide synthase (eNOS). Caveolin-1 (Cav1) inhibits eNOS function and NO production. Modifying Cav1 scaffold domain, in particular Phenylalanine at position 92 (F92) is critical for the inhibitory actions of Cav1 toward eNOS. The aims of this study were to investigate the effect of enhanced NO production in term of in vitro angiogenesis on rat bone marrow derived mesenchymal stem cells (BMSCs) transduced with a novel bicistronic lentiviral vector co-expressing eNOS and mutant Cav1 (F92A). A bicistronic eNOS/F92-Cav1 lentiviral vector was constructed, and used to transduce rat BMSCs. The expression of eNOS and VEGF protein were confirmed by western-blot. NO production was detected by the greiss assay and in vitro angiogenesis was assessed by matrigel assisted capillary tube formation. The cell viability was evaluated using a Cell Counting Kit (CCK)-8. The bicistronic eNOS/F92A-Cav1 lentiviral vector increased eNOS and VEGF protein expression, NO production compared to controls. In vitro capillary formation was increased in eNOS-F92A transduced cells and cell viability was not affected by transduction. Transduction of rat BMSCs with an eNOS-F92A-Cav1 lentivir...Continue Reading

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Citations

Oct 25, 2016·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Haiying ChenLexin Wang
Jan 26, 2017·Heart, Lung & Circulation·Hai-Ying ChenLe-Xin Wang
Jan 13, 2018·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Hai-Ying ChenLe-Xin Wang

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