The stimulatory effects of eNOS/F92A-Cav1 on NO production and angiogenesis in BMSCs.
作者： Peng Xia , Hai-ying Chen , Shuang-feng Chen , Lei Wang , Pádraig Michael Strappe
DOI: 10.1016/J.BIOPHA.2015.11.001
关键词:
摘要: Abstract Background Nitric oxide (NO) is generated in endothelial cells by nitric synthase (eNOS). Caveolin-1 (Cav1) inhibits eNOS function and NO production. Modifying Cav1 scaffold domain, particular Phenylalanine at position 92 (F92) critical for the inhibitory actions of toward eNOS. The aims this study were to investigate effect enhanced production term vitro angiogenesis on rat bone marrow derived mesenchymal stem (BMSCs) transduced with a novel bicistronic lentiviral vector co-expressing mutant (F92A). Methods A eNOS/F92-Cav1 was constructed, used transduce BMSCs. expression VEGF protein confirmed western-blot. detected greiss assay assessed matrigel assisted capillary tube formation. cell viability evaluated using Cell Counting Kit (CCK)-8. Results eNOS/F92A-Cav1 increased expression, compared controls. In formation eNOS-F92A not affected transduction. Conclusion Transduction BMSCs an eNOS-F92A-Cav1 can increase enhancing expression. did reduce viability. This demonstrates that genetic modification enhance producton could be applied based therapeutic approaches treat diseases such as pulmonary arterial hypertension (PAH) which characterized decreased release.
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