Microrna-26b attenuates monocrotaline-induced pulmonary vascular remodeling via targeting connective tissue growth factor (CTGF) and cyclin D1 (CCND1)
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Updated: Mar 19, 2026
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Ran Wang1, Xing Ding1, Sijing Zhou2
1Department of Respiratory Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.
Abstract:
MicroRNAs are involved in the control of cell growth, and deregulated pulmonary artery smooth muscle cell proliferation plays an essential role in the development of pulmonary hypertension. The objective of this study was to identify differentially expressed microRNA(s) and explore its therapeutic role in treatment of the disease. MicroRNA expression profile analysis showed microRNA-26b was differentially expressed in pulmonary artery smooth muscle cells harvested from monocrotaline-treated rats, and we validated microRNA-26b targets, in vitro and in vivo, CTGF and CCND1, both of which have been shown, in our previous work, to be involved in the pathogenesis of pulmonary hypertension. In vivo experiments demonstrated monocrotaline-induced pulmonary artery remodeling could be almost completely abolished by administration of microRNA-26b, while CTGF or CCND1 shRNA significantly, but only partially, attenuated the remodeling by silencing the designed target. Additionally, exogenous expression of the microRNA-26b substantially downregulated CTGF and CCND1 in human pulmonary artery smooth muscle cells. MicroRNA-26b might be a potent therapeutic tool to treat pulmonary hypertension.
Insights
MicroRNA-26b effectively treats pulmonary hypertension by downregulating cell growth factors CTGF and CCND1. This microRNA (miRNA) therapy shows promise in reversing pulmonary artery remodeling and offers a potential new treatment for this condition.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Pulmonary Hypertension Research
Background:
- Pulmonary hypertension involves uncontrolled smooth muscle cell proliferation.
- MicroRNAs regulate cell growth and are implicated in disease pathogenesis.
Purpose of the Study:
- Identify differentially expressed microRNAs in pulmonary hypertension.
- Investigate the therapeutic potential of microRNA-26b for pulmonary hypertension treatment.
Main Methods:
- MicroRNA expression profiling in monocrotaline-induced pulmonary hypertension rat model.
- Validation of microRNA-26b targets (CTGF, CCND1) in vitro and in vivo.
- Assessment of therapeutic efficacy of microRNA-26b and target gene silencing (shRNA) on pulmonary artery remodeling.
Main Results:
- MicroRNA-26b was significantly downregulated in pulmonary artery smooth muscle cells of affected rats.
- MicroRNA-26b administration abolished monocrotaline-induced pulmonary artery remodeling.
- Silencing CTGF or CCND1 partially attenuated pulmonary artery remodeling.
- Exogenous microRNA-26b downregulated CTGF and CCND1 in human pulmonary artery smooth muscle cells.
Conclusions:
- MicroRNA-26b is a key regulator in pulmonary hypertension pathogenesis.
- MicroRNA-26b demonstrates significant therapeutic potential for pulmonary hypertension.
- Targeting microRNA-26b offers a promising therapeutic strategy for pulmonary hypertension.
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