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miR-29a-3p/THBS2 Axis Regulates PAH-Induced Cardiac Fibrosis
Chih-Hsin Hsu1, I-Fan Liu2,3, Hsuan-Fu Kuo4,5,6,7
1Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 704, Taiwan.
Abstract:
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.
Insights
MicroRNA-29a-3p (miR-29a-3p) shows anti-fibrotic effects in pulmonary artery hypertension (PAH) by targeting thrombospondin-2 (THBS2). Lower miR-29a-3p and higher THBS2 levels indicate PAH progression and may serve as prognostic markers.
Area of Science:
- Biomedical research
- Cardiovascular pathology
- Molecular biology
Background:
- Pulmonary artery hypertension (PAH) is characterized by extracellular matrix (ECM) remodeling and cardiac fibrosis.
- MicroRNA-29a-3p (miR-29a-3p) is known to regulate ECM in other fibrotic conditions, but its role in PAH-induced cardiac fibrosis is not well understood.
- Thrombospondin-2 (THBS2) is an ECM protein implicated in fibrosis.
Purpose of the Study:
- To investigate the role of miR-29a-3p in cardiac fibrosis progression in PAH.
- To determine the relationship between miR-29a-3p and THBS2 expression in PAH.
- To evaluate the diagnostic and prognostic value of miR-29a-3p and THBS2 in PAH.
Main Methods:
- Assessed miR-29a-3p and THBS2 expression in cell culture, a monocrotaline-induced PAH mouse model, and human PAH patients.
- Investigated the direct targeting of THBS2 by miR-29a-3p.
- Correlated circulating levels of miR-29a-3p and THBS2 with PAH diagnostic parameters.
Main Results:
- Circulating levels of miR-29a-3p were decreased, while THBS2 levels were increased in patients and mice with PAH.
- miR-29a-3p directly targets THBS2, inhibiting its expression.
- miR-29a-3p demonstrated a direct anti-fibrotic effect on PAH-induced cardiac fibrosis.
- Circulating miR-29a-3p and THBS2 levels correlated with PAH diagnostic parameters, indicating prognostic value.
Conclusions:
- miR-29a-3p acts as a direct regulator of THBS2 in PAH-induced cardiac fibrosis.
- miR-29a-3p exhibits anti-fibrotic properties relevant to PAH.
- Circulating miR-29a-3p and THBS2 hold potential as diagnostic and prognostic biomarkers for PAH, with miR-29a-3p showing therapeutic promise.
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