microRNA-637/661 ameliorate hypoxic-induced pulmonary arterial hypertension by targeting TRIM29 signaling pathway

Sci Rep. 2024 Nov 14;14(1):27971. doi: 10.1038/s41598-024-79769-2.

Abstract

The pathogenesis of pulmonary arterial hypertension (PAH) is closely linked to the abnormal proliferation of pulmonary artery smooth muscle cells. Studies have demonstrated that microRNAs play pivotal roles in the progression of pulmonary hypertension. We found that microRNA-637 (miR-637) and microRNA-661 (miR-661) are expressed at low levels in the serum of PAH patients. Moreover, the overexpression of miR-637 or miR-661 inhibited human pulmonary artery smooth muscle cell (HPASMC) proliferation and migration in hypoxic culture. Mechanistically, we overexpressed these two microRNAs in HPASMCs, and the RNA-sequencing (RNA-seq) results demonstrated that TRIM29 mRNA was suppressed, indicating that TRIM29 is a substrate. TRIM29 accumulates in the serum of patients with PAH and promotes cell proliferation and migration by activating AKT/mTOR signalling. In addition, overexpression of miR-637 or miR-661 reversed TRIM29-mediated HPASMC proliferation and migration. This study revealed that miR-637 and miR-661 are able to inhibit the proliferation ability of HPASMCs under hypoxic conditions through targeting TRIM29, suggesting that the microRNA-637/661/TRIM29 axis may act as a target for PAH treatment.

Keywords: AKT/mTOR signalling; Pulmonary arterial hypertension; RNA-seq; TRIM29; microRNA.

MeSH terms

  • Cell Hypoxia
  • Cell Movement* / genetics
  • Cell Proliferation*
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Female
  • Humans
  • Hypertension, Pulmonary / genetics
  • Hypertension, Pulmonary / metabolism
  • Hypoxia / genetics
  • Hypoxia / metabolism
  • Male
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Myocytes, Smooth Muscle / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Pulmonary Arterial Hypertension / genetics
  • Pulmonary Arterial Hypertension / metabolism
  • Pulmonary Arterial Hypertension / pathology
  • Pulmonary Artery / metabolism
  • Pulmonary Artery / pathology
  • Signal Transduction*
  • Transcription Factors* / genetics
  • Transcription Factors* / metabolism

Substances

  • MicroRNAs
  • Transcription Factors
  • MIRN637 microRNA, human
  • DNA-Binding Proteins
  • Proto-Oncogene Proteins c-akt