BACKGROUND: Abnormal proliferation of PASMCs is the main phenotype of pulmonary arterial hypertension (PAH). MicroRNAs (miRNAs) were reported to participate in regulating the progression of PAH. Here, we aimed to investigate the impact of miR-107 on proliferation and migration of PASMCs and potential mechanism. METHODS: MTT assay was carried out to examine the cell viability of PASMCs. PASMC migration ability was verified through Transwell assay. RT-qPCR was performed to detect the expression of miR-107 and NOR1. Western blot was conducted to detect the expression of cell proliferation markers Ki-67, p27 and Cyclin D1, as well as NOR1. Bioinformatics analysis was conducted to verify whether the 3'-untranslated region (3'-UTR) of NOR1 contains a binding site for miR-107, and luciferase reporter assay and RNA immunoprecipitation (RIP) were employed to confirm the relationship between miR-107 and NOR1. RESULTS: Platelet-derived growth factor (PDGF)-BB promoted the cell viability and migration of PASMCs, and suppressed miR-107 expression in a time-dependent and concentration-dependent manner. Introduction of miR-107 inhibited the promotion of proliferation and migration of PASMCs stimulated by PDGF-BB, while loss of miR-107 facilitated PDGF-BB-induced promoted effects. NOR1 was identified as a downstream gene of miR-107 and down-regulated by miR-107. Knockout of NOR1 also repressed the promotion of proliferation and migration of PASMCs stimulated by PDGF-BB. Additionally, restoration of NOR1 attenuated the inhibition of miR-107 on the cell viability and migration ability of PASMCs. CONCLUSION: miR-107 inhibits PDGF-BB-induced PASMCs proliferation and migration through targeting NOR1. IJCEP
BACKGROUND: Abnormal proliferation of PASMCs is the main phenotype of pulmonary arterial hypertension (PAH). MicroRNAs (miRNAs) were reported to participate in regulating the progression of PAH. Here, we aimed to investigate the impact of miR-107 on proliferation and migration of PASMCs and potential mechanism. METHODS:MTT assay was carried out to examine the cell viability of PASMCs. PASMC migration ability was verified through Transwell assay. RT-qPCR was performed to detect the expression of miR-107 and NOR1. Western blot was conducted to detect the expression of cell proliferation markers Ki-67, p27 and Cyclin D1, as well as NOR1. Bioinformatics analysis was conducted to verify whether the 3'-untranslated region (3'-UTR) of NOR1 contains a binding site for miR-107, and luciferase reporter assay and RNA immunoprecipitation (RIP) were employed to confirm the relationship between miR-107 and NOR1. RESULTS: Platelet-derived growth factor (PDGF)-BB promoted the cell viability and migration of PASMCs, and suppressed miR-107 expression in a time-dependent and concentration-dependent manner. Introduction of miR-107 inhibited the promotion of proliferation and migration of PASMCs stimulated by PDGF-BB, while loss of miR-107 facilitated PDGF-BB-induced promoted effects. NOR1 was identified as a downstream gene of miR-107 and down-regulated by miR-107. Knockout of NOR1 also repressed the promotion of proliferation and migration of PASMCs stimulated by PDGF-BB. Additionally, restoration of NOR1 attenuated the inhibition of miR-107 on the cell viability and migration ability of PASMCs. CONCLUSION:miR-107 inhibits PDGF-BB-induced PASMCs proliferation and migration through targeting NOR1. IJCEP