ArticleMedical science monitor : international medical journal of experimental and clinical research2016
Upregulated miR-17 Regulates Hypoxia-Mediated Human Pulmonary Artery Smooth Muscle Cell Proliferation and Apoptosis by Targeting Mitofusin 2.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 79 citations in OpenAlex.
- LncRNA H19 promotes vascular remodeling by inhibiting MFN2.Functional & integrative genomics · 2026Article
- Mitochondrial acid-sensing ion channel 1a deficiency induces mitochondrial dysfunction in pulmonary arterial smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- miR-17-5p: bridging the gap between disease mechanisms and therapeutic innovations.Epigenomics · 2025Review
- Emerging insights into pulmonary hypertension: the potential role of mitochondrial dysfunction and redox homeostasis.Molecular and cellular biochemistry · 2025Review
- HNRNPA2B1: a novel target in pulmonary arterial hypertension.Frontiers in cardiovascular medicine · 2025Review
- Targeting mitochondrial quality control: new therapeutic strategies for major diseases.Military Medical Research · 2024Review
- MicroRNA Monitoring in Human Alveolar Macrophages from Patients with Smoking-Related Lung Diseases: A Preliminary Study.Biomedicines · 2024Article
- Novel Relationship between Mitofusin 2-Mediated Mitochondrial Hyperfusion, Metabolic Remodeling, and Glycolysis in Pulmonary Arterial Endothelial Cells.International journal of molecular sciences · 2023Article
- Unraveling the epigenetic landscape of pulmonary arterial hypertension: implications for personalized medicine development.Journal of translational medicine · 2023Review
- Targeting Mitochondrial Metabolic Dysfunction in Pulmonary Hypertension: Toward New Therapeutic Approaches?International journal of molecular sciences · 2023Review
- Mitochondria in hypoxic pulmonary hypertension, roles and the potential targets.Frontiers in physiology · 2023Review
- Microrna-486-5P Regulates Human Pulmonary Artery Smooth Muscle Cell Migration via Endothelin-1.International journal of molecular sciences · 2022Article
- Integrated analysis of tRNA-derived small RNAs in proliferative human aortic smooth muscle cells.Cellular & molecular biology letters · 2022Article
- Proteasome Inhibitors Decrease the Viability of Pulmonary Arterial Smooth Muscle Cells by Restoring Mitofusin-2 Expression under Hypoxic Conditions.Biomedicines · 2022Article
- MiR-34a-3p suppresses pulmonary vascular proliferation in acute pulmonary embolism rat by targeting DUSP1.Bioscience reports · 2022Article
- Bioactivities and mechanisms of natural medicines in the management of pulmonary arterial hypertension.Chinese medicine · 2022Review
- Mitochondrial dysfunction in pulmonary arterial hypertension.Frontiers in physiology · 2022Review
- Mechanism of Hypoxia-Mediated Smooth Muscle Cell Proliferation Leading to Vascular Remodeling.BioMed research international · 2022Review
- The roles of microRNAs played in lung diseases via regulating cell apoptosis.Molecular and cellular biochemistry · 2021Review
- Carbonic Anhydrase III Attenuates Hypoxia-Induced Apoptosis and Activates PI3K/Akt/mTOR Pathway in H9c2 Cardiomyocyte Cell Line.Cardiovascular toxicology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Pulmonary arterial hypertension (PAH) is a fatal disease characterized by impaired regulation of pulmonary artery vascular growth and remodeling. Aberrant expression of miR-17 has been shown to be involved in the pathogenesis of PAH, but its underlying molecular mechanism has not been elucidated. MATERIAL AND METHODS Mitofusin 2 (MFN2) expression was determined by qRT-PCR. The protein expression levels of MFN2, proliferating cell nuclear antigen (PCNA), and pro-apoptotic protein cleaved Caspase-3 were measured using Western blot analysis. Cell proliferation and apoptosis were assessed by CellTiter-Glo reagent and flow cytometry, respectively. Caspase-3/7 activity was measured using an Apo-ONE Homogeneous Caspase-3/7 assay kit. The regulation of miR-17 on MFN2 expression was assessed using luciferase reporter assay system. RESULTS miR-17 expression was upregulated in human pulmonary artery smooth muscle cells (hPASMCs) treated with hypoxia and lung tissues of PAH patients. Inhibition of miR-17 suppressed hypoxia-induced proliferation and promoted apoptosis in hPASMCs. miR-17 inhibited MFN2 expression by binding to its 3'-UTR. Decreased cell viability and increased apoptosis and Caspase-3 activity were observed in the anti-miR-17 + siNC group compared with the anti-miR-NC + siNC group. The expression of cleaved Caspase-3 was upregulated and the expression of PCNA was downregulated in the anti-miR-17 + siNC group. Moreover, these alterations were attenuated by knockdown of MFN2. CONCLUSIONS miR-17 regulates proliferation and apoptosis in hPASMCs through MFN2 modulation. We found that miR-17 acts as a potential regulator of proliferation and apoptosis of hPASMCs, and that it might be developed as a promising new strategy for the treatment of PAH.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.