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MALAT1 promoted cell proliferation and migration via MALAT1/miR‐155/MEF2A pathway in hypoxia of cardiac stem cells
Author(s) -
Wang Qiuyun,
Lu Guoping,
Chen Zhenyue
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.27925
Subject(s) - malat1 , hypoxia (environmental) , cell growth , microrna , cancer research , cell , gene knockdown , cell migration , chemistry , microbiology and biotechnology , biology , downregulation and upregulation , biochemistry , apoptosis , gene , long non coding rna , organic chemistry , oxygen
Accumulating evidence revealed that hypoxia contributed to many human diseases, including ischemic myocardium and heart failure (HF). In recent years, the roles of hypoxia in stem cell survival and cardiac biology have been studied extensively. However, the underlying molecular mechanisms remain to be elucidated. As a leading cause of HF, ischemic heart disease was correlated with hypoxia. In this study, we firstly constructed the hypoxia cell model by CoCl 2 in cardiac stem cells (CSCs) and found that hypoxia induced the cell proliferation and migration potential in CSCs. Then, we demonstrated that the expression of metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) was promoted in CoCl 2 ‐induced CSCs hypoxia model. Furthermore, we found that knockdown of MALAT1 inhibited the cell proliferation and migration in CoCl 2 ‐induced CSCs hypoxia model. In addition, we revealed that MALAT1 regulated the microRNA‐155 (miR‐155) expression in CSCs under both the normal and hypoxia conditions and further, manipulation of the miR‐155 expression affected the role of MALAT1 in CoCl 2 ‐induced CSCs hypoxia cell model. We then illustrated that miR‐155 regulated the myocyte enhancer factor 2A (MEF2A) expression in CSCs under both the normal and hypoxia conditions and further, changing the expression of MEF2A affected the role of miR‐155. Finally, we demonstrated that MALAT1 regulated the MEF2A expression and exerted its role via modulation of the MALAT1/miR‐155/MEF2A pathway. Taken together, our study illustrated that MALAT1 promoted the cell proliferation and migration in CoCl 2 ‐induced CSCs hypoxia model, acting mechanistically by promoting MEF2A expression via “sponging” miR‐155.