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MicroRNA-126 affects cell apoptosis, proliferation, cell cycle and modulates VEGF/TGF-β levels in pulmonary artery endothelial cells.

Abstract

OBJECTIVE

In the clinic, therapeutic options for pulmonary arterial hypertension are limited; therefore, investigating the therapeutic strategies and novel therapies is critical for pulmonary arterial hypertension (PAH) treatment. This study aimed to evaluate the role of miRNA-126 (miR-126) and its associated signaling pathways and specific mechanisms for the pathogenesis of PAH.

MATERIALS AND METHODS

The pulmonary artery endothelial cells (PAECs) were isolated and identified. The miR-126 mimic and miR-126 inhibitor were synthesized. LV-3-miR-126 mimic viral vector and LV-3-miR-126 inhibitor vector were established and infected into pulmonary artery endothelial cells. Expression of sprouty-related EVH1 domain-containing protein 1 (SPRED1), phosphoinositide-3-kinase regulatory subunit 2 (PIK3R2) and miR-126 were detected using Real-time PCR (RT-PCR). Cell apoptosis (Annexin V-PE/7-AAD) and proliferation (PKH26) were examined by using FACScan flow cytometry. Vascular endothelial growth factor (VEGF), transforming growth factor β1 (TGF-β1) and TGF-β3 levels were evaluated using enzyme-linked immunosorbent assay (ELISA) kits.

RESULTS

miR-126 inhibited the endothelial cells related to SPRED1 and PIK3R2 expression. Over-expression of miR-126 significantly inhibited the PAECs apoptosis compared to PAECs and blank LV-3 vector group (p<0.05). miR-126 significantly triggered the PAECs proliferation compared to PAECs and blank LV-3 vector group (p<0.05). In functional analysis, miR-126 mimic significantly increased the cells amounts of S phases compared to PAECs and blank LV-3 vector group (p<0.05). Pre-infection with miR-126 mimic significantly enhanced the levels of VEGF, TGF-β1, and TGF-β3 compared to PAECs and blank LV-3 vector group (p<0.05).

CONCLUSIONS

miR-126 could affect cell apoptosis, proliferation, cell cycle, and modulate VEGF/TGF-β levels.

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  • Authors+Show Affiliations

    ,

    Department of Cardiovascular Surgery, Daping Hospital, Army Medical University, Chongqing, China. zhongqianjin@hainan.net.

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    Source

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    31002170

    Citation

    Yuan, Y, et al. "MicroRNA-126 Affects Cell Apoptosis, Proliferation, Cell Cycle and Modulates VEGF/TGF-β Levels in Pulmonary Artery Endothelial Cells." European Review for Medical and Pharmacological Sciences, vol. 23, no. 7, 2019, pp. 3058-3069.
    Yuan Y, Shen C, Zhao SL, et al. MicroRNA-126 affects cell apoptosis, proliferation, cell cycle and modulates VEGF/TGF-β levels in pulmonary artery endothelial cells. Eur Rev Med Pharmacol Sci. 2019;23(7):3058-3069.
    Yuan, Y., Shen, C., Zhao, S. L., Hu, Y. J., Song, Y., & Zhong, Q. J. (2019). MicroRNA-126 affects cell apoptosis, proliferation, cell cycle and modulates VEGF/TGF-β levels in pulmonary artery endothelial cells. European Review for Medical and Pharmacological Sciences, 23(7), pp. 3058-3069. doi:10.26355/eurrev_201904_17588.
    Yuan Y, et al. MicroRNA-126 Affects Cell Apoptosis, Proliferation, Cell Cycle and Modulates VEGF/TGF-β Levels in Pulmonary Artery Endothelial Cells. Eur Rev Med Pharmacol Sci. 2019;23(7):3058-3069. PubMed PMID: 31002170.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - MicroRNA-126 affects cell apoptosis, proliferation, cell cycle and modulates VEGF/TGF-β levels in pulmonary artery endothelial cells. AU - Yuan,Y, AU - Shen,C, AU - Zhao,S-L, AU - Hu,Y-J, AU - Song,Y, AU - Zhong,Q-J, PY - 2019/4/20/entrez SP - 3058 EP - 3069 JF - European review for medical and pharmacological sciences JO - Eur Rev Med Pharmacol Sci VL - 23 IS - 7 N2 - OBJECTIVE: In the clinic, therapeutic options for pulmonary arterial hypertension are limited; therefore, investigating the therapeutic strategies and novel therapies is critical for pulmonary arterial hypertension (PAH) treatment. This study aimed to evaluate the role of miRNA-126 (miR-126) and its associated signaling pathways and specific mechanisms for the pathogenesis of PAH. MATERIALS AND METHODS: The pulmonary artery endothelial cells (PAECs) were isolated and identified. The miR-126 mimic and miR-126 inhibitor were synthesized. LV-3-miR-126 mimic viral vector and LV-3-miR-126 inhibitor vector were established and infected into pulmonary artery endothelial cells. Expression of sprouty-related EVH1 domain-containing protein 1 (SPRED1), phosphoinositide-3-kinase regulatory subunit 2 (PIK3R2) and miR-126 were detected using Real-time PCR (RT-PCR). Cell apoptosis (Annexin V-PE/7-AAD) and proliferation (PKH26) were examined by using FACScan flow cytometry. Vascular endothelial growth factor (VEGF), transforming growth factor β1 (TGF-β1) and TGF-β3 levels were evaluated using enzyme-linked immunosorbent assay (ELISA) kits. RESULTS: miR-126 inhibited the endothelial cells related to SPRED1 and PIK3R2 expression. Over-expression of miR-126 significantly inhibited the PAECs apoptosis compared to PAECs and blank LV-3 vector group (p<0.05). miR-126 significantly triggered the PAECs proliferation compared to PAECs and blank LV-3 vector group (p<0.05). In functional analysis, miR-126 mimic significantly increased the cells amounts of S phases compared to PAECs and blank LV-3 vector group (p<0.05). Pre-infection with miR-126 mimic significantly enhanced the levels of VEGF, TGF-β1, and TGF-β3 compared to PAECs and blank LV-3 vector group (p<0.05). CONCLUSIONS: miR-126 could affect cell apoptosis, proliferation, cell cycle, and modulate VEGF/TGF-β levels. SN - 2284-0729 UR - https://www.unboundmedicine.com/medline/citation/31002170/MicroRNA-126_affects_cell_apoptosis,_proliferation,_cell_cycle_and_modulates_VEGF/TGF-β_levels_in_pulmonary_artery_endothelial_cells L2 - https://www.europeanreview.org/article/17588 DB - PRIME DP - Unbound Medicine ER -