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Involvement of miR‐200b–PKCα signalling in pulmonary hypertension in cor pulmonale model
Author(s) -
Qian Xiaojun,
Zhao Hongqin,
Feng Qiuting
Publication year - 2020
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13213
Subject(s) - ventricle , pulmonary hypertension , pulmonary artery , lung , right ventricular hypertrophy , muscle hypertrophy , pulmonary fibrosis , medicine , cardiology , protein kinase c , fibrosis , western blot , pathology , biology , kinase , gene , microbiology and biotechnology , biochemistry
The right ventricle (RV) enlargement and pulmonary fibrosis are involved in cor pulmonale. The role of miR‐200b in cor pulmonale is less well understood. This study was designed to evaluate the regulatory roles of miR‐200b in cor pulmonale. Cor pulmonary mouse model was built via monocrotaline injection of monocrotaline (MCT). The expression of miR‐200b in the lungs, RV and left ventricle (LV) are using real‐time polymerase chain reaction. The transthoracic echocardiography was employed to determine the effects of miR‐200b mimics and Gö6976 injection on MCT mice. The protein levels of protein kinase C α (PKCα), collagen, and fibronectin in the lung, RV, and LV in the mice with and without miR‐200b mimics and Gö6976 injection were evaluated using western blot. The expression of miR‐200b decreased in MCT mice, while there was no difference in LV. Both the miR‐200b mimics and Gö6976 injection reversed the muscularization in the pulmonary artery, reversed RV hypertrophy, reduced RV systolic pressure, wall thickness and pulmonary fibrosis. The injection of miR‐200b can reduce the PKCα expression in the lung, RV, and LV. This study confirmed the down‐regulation of miR‐200b in cor pulmonale. The reverse effects of miR‐200b in the present study may provide a potential tool for cor pulmonary treatment.