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Retracted : Upregulated microRNA‐132 rescues cardiac fibrosis and restores cardiocyte proliferation in dilated cardiomyopathy through the phosphatase and tensin homolog–mediated PI3K/Akt signal transduction pathway
Author(s) -
Zhang ChenJun,
Huang Yu,
Lu JiDe,
Lin Jie,
Ge ZhiRu,
Huang Hui
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27081
Subject(s) - tensin , pten , protein kinase b , pi3k/akt/mtor pathway , fibrosis , cancer research , biology , myocardial fibrosis , signal transduction , cardiac fibrosis , cell growth , apoptosis , endocrinology , microbiology and biotechnology , medicine , biochemistry
Cardiac fibrosis is known to be present in dilated cardiomyopathy (DCM) and it predicts the occurrence of sudden death and congestive heart failure. The aim of our study is to investigate the expression of microRNA‐132 (miR‐132) and its effect on cardiocyte proliferation, apoptosis, and cardiac fibrosis by binding to phosphatase and tensin homolog (PTEN) through the phosphateidylinositol 3‐kinase (PI3K)/protein kinase (Akt) signal transduction pathway in DCM rats. DCM rat models induced by doxorubicin were established and confirmed by an ultrasonic cardiogram. Epithelial cells were treated with inhibitors, activators, and small interfering RNAs to identify the mechanisms by which miR‐132 controls cardiocyte activity and cardiac fibrosis. Angiotensin II (Ang II) and aldosterone (ALD) expressions were detected by an enzyme‐linked immunosorbent assay. The relationship between PTEN and miR‐132 was verified by a dual‐luciferase reporter assay. Cell proliferation and apoptosis were tested by the MTT assay and flow cytometry. PTEN was determined to be the target gene of miR‐132. Rat models of DCM exhibited a lower level of miR‐132, PI3K, Akt, B‐cell lymphoma 2, collagen I, and collagen III, but a higher level of PTEN, Bcl‐2–associated X protein, and proliferating cell nuclear antigen as well as inflammatory response (Ang II and ALD), accompanied by declined cardiocyte proliferation and elevated apoptosis and cardiac fibrosis. Upregulated miR‐132 or silenced PTEN activated the PI3K/Akt pathway, thus facilitating cardiocyte proliferation and repressing cardiocyte apoptosis and cardiac fibrosis, as well as inflammatory responses. Downregulated miR‐132 reversed this tendency. These findings indicate that miR‐132 activates the PI3K/Akt pathway by inhibiting PTEN expression, thus facilitating cardiocyte proliferation and inhibiting apoptosis and cardiac fibrosis in DCM rats.