ArticleInternational journal of molecular medicine2020
MicroRNA‑15a‑5p induces pulmonary artery smooth muscle cell apoptosis in a pulmonary arterial hypertension model via the VEGF/p38/MMP‑2 signaling pathway.
Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- β-sitosterol Alleviates Pulmonary Arterial Hypertension in Rats With Involvement of the VEGF/PI3K/AKT Signaling Pathway.Pulmonary circulation · 2026Article
- Placental miRNA profiling in assisted reproductive technology (ART) pregnancies.Journal of assisted reproduction and genetics · 2025Article
- miRNAs in Pulmonary Hypertension: Mechanistic Insights and Therapeutic Potential.Biomedicines · 2025Review
- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- Article
- Article
- Cell Death in Pulmonary Arterial Hypertension.International journal of medical sciences · 2024Review
- Genetic and epigenetic factors of arterial hypertension: a bibliometric- and in-silico-based analyses.Frontiers in molecular biosciences · 2023Review
- Epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension.Frontiers in immunology · 2023Review
- MiR-15a-5p accelerated vascular smooth muscle cells viabilities and migratory abilities via targeting Bcl-2.Physiological research · 2022Article
- MicroRNA miR-627-5p restrains pulmonary artery smooth muscle cell dysfunction by targeting MAP 2 K4 and PI3K/AKT signaling.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2022Article
- Article
- The roles of microRNAs played in lung diseases via regulating cell apoptosis.Molecular and cellular biochemistry · 2021Review
- Circular RNA circFADS2 is overexpressed in sepsis and suppresses LPS-induced lung cell apoptosis by inhibiting the maturation of miR-15a-5p.BMC immunology · 2021Article
- Non-Coding RNA Networks in Pulmonary Hypertension.Frontiers in genetics · 2021Review
- The Function of microRNAs in Pulmonary Embolism: Review and Research Outlook.Frontiers in pharmacology · 2021Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the role of microRNA‑15a‑5p (miR‑15a‑5p) in pulmonary arterial hypertension (PAH) and elucidate the underlying pro‑apoptotic mechanism. Reverse transcription‑quantitative PCR analysis and gene microarray hybridization were used to measure the expression of miR‑15a‑5p in the lung tissues of rats with monocrotaline (MCT)‑induced PAH. Flow cytometry and caspase‑3/9 activity assays were adopted to measure the apoptosis of pulmonary artery smooth muscle cells (PASMCs). The expression of apoptosis‑related proteins was analyzed using western blotting. The results demonstrated that the expression of miR‑15a‑5p was significantly increased in the lung tissues of rats with MCT‑induced PAH. In addition, the overexpression of miR‑15a‑5p reduced PASMC proliferation, induced apoptosis, promoted the activity of caspase‑3/9, induced the protein expression of B‑cell lymphoma 2‑associated X protein (Bax), decreased the expression of B‑cell lymphoma 2 (Bcl‑2), increased inflammation, as indicated by the expression of tumor necrosis factor‑α (TNF)‑α and interleukin (IL)‑1β, IL‑6 and IL‑18, suppressed the protein expression of vascular endothelial growth factor (VEGF), and promoted the protein expression levels of phosphorylated (p)‑p38 mitogen‑activated protein kinase (p38) and matrix metalloproteinase (MMP)‑2 in the PASMCs of rats with MCT‑induced PAH. By contrast, the downregulation of miR‑15a‑5p increased cell proliferation, decreased apoptosis, reduced the activity of caspase‑3/9 and the protein expression of Bax, increased the expression of Bcl‑2, inhibited inflammation (as suggested by the expression of TNF‑α, IL‑1β, IL‑6 and IL‑18), induced the protein expression of VEGF, and suppressed the protein expression of p‑p38 and MMP‑2 in the PASMCs of rats with MCT‑induced PAH. The inhibition of VEGF attenuated the effects of the overexpression of miR‑15a‑5p on the inhibition of cell proliferation, apoptotic rate, caspase‑3/9 activity and protein expression of Bax, and it attenuated the increased inflammation, as indicated by the protein expression of p38 and MMP‑2 in the PASMCs. In conclusion, the data of the present study demonstrated that miR‑15a‑5p induced the apoptosis of PASMCs in an animal model of PAH via the VEGF/p38/MMP‑2 signaling pathway. However, further research is required to fully elucidate the role of miR‑15a‑5p in the development of PAH.
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