Yun Zhou1, Xuan-Liang Fang2, Yun Zhang3, Yan-Ni Feng4, Shan-Shan Wang5. 1. Department of Emergency, The Affiliated Hospital of Medical School of Ningbo University, Ningbo City, Zhejiang Province, China. 2. Department of Orthopedics, Ningbo City, Zhejiang Province, China. 3. Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Medical School of Ningbo University, Ningbo City, Zhejiang Province, China. 4. Department of Emergency, Ningbo Seventh Hospital, Ningbo City, Zhejiang Province, China. 5. Intensive Care Unit, The Affiliated Hospital of Medical School of Ningbo University, Ningbo City, Zhejiang Province, China.
Abstract
BACKGROUND: The function of miR-20a-5p in pulmonary artery smooth muscle cells (PASMCs) and the underlying mechanism remains largely unknown. METHODS: C57BL/6J mice and PASMCs were used for constructing pulmonary artery hypertension (PAH) animal and cell models, respectively. Reverse transcription polymerase chain reaction (RT-PCR) was employed to detect miR-20a-5p and ATP-binding cassette subfamily A member 1 (ABCA1) messenger RNA expression. CCK-8, Transwell, and TUNEL experiments were used to determine PASMCs proliferation, migration, and apoptosis. The relationship between miR-20a-5p and ABCA1 was detected by luciferase reporter experiment, Western blot analysis, and qRT-PCR. RESULTS: miR-20a-5p was remarkably elevated in PASMCs of PAH mice and human PASMCs treated by hypoxia, while ABCA1 was remarkably decreased. After transfection of miR-20a-5p mimics, PASMCs proliferation and migration were promoted and PASMCs apoptosis was suppressed. ABCA1 was confirmed to be a target of miR-20a-5p and restoration of ABCA1 reversed the function of miR-20a-5p. CONCLUSION: miR-20a-5p enhances the proliferation and migration of PASMCs to promote the development of PAH via targeting ABCA1.
BACKGROUND: The function of miR-20a-5p in pulmonary artery smooth muscle cells (PASMCs) and the underlying mechanism remains largely unknown. METHODS: C57BL/6J mice and PASMCs were used for constructing pulmonary artery hypertension (PAH) animal and cell models, respectively. Reverse transcription polymerase chain reaction (RT-PCR) was employed to detect miR-20a-5p and ATP-binding cassette subfamily A member 1 (ABCA1) messenger RNA expression. CCK-8, Transwell, and TUNEL experiments were used to determine PASMCs proliferation, migration, and apoptosis. The relationship between miR-20a-5p and ABCA1 was detected by luciferase reporter experiment, Western blot analysis, and qRT-PCR. RESULTS:miR-20a-5p was remarkably elevated in PASMCs of PAH mice and human PASMCs treated by hypoxia, while ABCA1 was remarkably decreased. After transfection of miR-20a-5p mimics, PASMCs proliferation and migration were promoted and PASMCs apoptosis was suppressed. ABCA1 was confirmed to be a target of miR-20a-5p and restoration of ABCA1 reversed the function of miR-20a-5p. CONCLUSION:miR-20a-5p enhances the proliferation and migration of PASMCs to promote the development of PAH via targeting ABCA1.