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Hsu, Chih-Hsin; Liu, I-Fan; Kuo, Hsuan-Fu; Li, Chia-Yang; Lian, Wei-Shiung; Chang, Chia-Yuan; Chen, Yung-Hsiang; Liu, Wei-Lun; Lu, Chi-Yu; Liu, Yu-Ru; Lin, Tzu-Chieh; Lee, Tsung-Ying; Huang, Chi-Yuan; Hsieh, Chong-Chao; Liu, Po-Len
International journal of molecular sciences, 10/2021, Volume: 22, Issue: 19Journal Article
Pulmonary artery hypertension (PAH) pathology involves extracellular matrix (ECM) remodeling in cardiac tissues, thus promoting cardiac fibrosis progression. miR-29a-3p reportedly inhibits lung progression and liver fibrosis by regulating ECM protein expression; however, its role in PAH-induced fibrosis remains unclear. In this study, we aimed to investigate the role of miR-29a-3p in cardiac fibrosis progression in PAH and its influence on ECM protein thrombospondin-2 (THBS2) expression. The diagnostic and prognostic values of miR-29a-3p and THBS2 in PAH were evaluated. The expressions and effects of miR-29a-3p and THBS2 were assessed in cell culture, monocrotaline-induced PAH mouse model, and patients with PAH. The levels of circulating miR-29a-3p and THBS2 in patients and mice with PAH decreased and increased, respectively. miR-29a-3p directly targets THBS2 and regulates THBS2 expression via a direct anti-fibrotic effect on PAH-induced cardiac fibrosis. The circulating levels of miR-29a-3p and THBS2 were correlated with PAH diagnostic parameters, suggesting their independent prognostic value. miR-29a-3p targeted THBS2 expression via a direct anti-fibrotic effect on PAH-induced cardiac fibrosis, indicating miR-29a-3p acts as a messenger with promising therapeutic effects.
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