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Network of three specific microRNAs influence type 2 diabetes through inducing insulin resistance in muscle cell lines
Author(s) -
Honardoost Maryam,
Keramati Farid,
Arefian Ehsan,
Mohammadi Yeganeh Samira,
Soleimani Masoud
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.27381
Subject(s) - insulin resistance , downregulation and upregulation , transfection , microbiology and biotechnology , microrna , biology , protein kinase a , insulin , kinase , cell culture , endocrinology , gene , biochemistry , genetics
Insulin resistance has been implicated as one of the best predictors for type 2 diabetes. Growing evidence propose the involvement of microRNAs (miRNAs) as short regulatory molecules in modulating and inducing resistance. In this regard, we have investigated the role of three selected miRNAs in insulin resistance development (miR‐135, miR‐202, and miR‐214), via assessing glucose uptake levels in C2C12 and L6 muscle cell lines. Interestingly, miRNA‐transfected cells demonstrated a significantly different glucose uptake compared to the positive control cells. In addition, we evaluated the expression levels of three putative miRNA target genes (Rho‐associated coiled‐coil containing protein kinase 1, serine/threonine kinase 2, and vesicle‐associated membrane protein 2) in transfected cells, recruiting luciferase assay. Our results indicated the targeting and downregulation of Rho‐associated coiled‐coil containing protein kinase 1 and serine/threonine kinase 2 genes in all miR‐transfected cell lines ( P ≤ 0.05), but not for vesicle‐associated membrane protein 2. MiRNA upregulation led to the poor stimulation of glucose uptake through insulin and developed insulin‐resistant phenotype in both muscle cell lines. Our study showed the role of three miRNAs in the induction of insulin resistance in cell lines and making them prone to type 2 diabetes development.