Abstract
Differentiation of 3T3-L1 cells into adipocytes involves a highly-orchestrated series of events including contact inhibition (CI), clonal expansion, growth arrest, and terminal differentiation. Recent study demonstrated that 3T3-L1 preadipocytes will not be differentiated into mature adipocytes without CI stage, which indicated that CI stage plays an important role during 3T3-L1 adipogenesis. However, the molecular mechanism is not yet fully understood. In the present study, we found that the expression level of miR-29a/b/c was decreased and the expression of DNMT3A was up-regulated during CI stage, respectively. Furthermore, overexpression of miR-29a/b/c during CI stage inhibits adipogenesis significantly but not at other stages. In addition, miR-29a/b/c repressed DNMT3A expression by directly targeting its 3’ untranslated region (3’ UTR). Our data reveal a novel mechanism of miR-29a/b/c in the regulation of adipogenesis.
Highlights
The prevalence of overweight and obesity in developed and developing countries has greatly increased the risk of insulin resistance and type 2 diabetes mellitus
The results demonstrated that more 3T3-L1 cells were differentiated into adipocytes when they stayed in CI stage longer, whereas adipocytes were rarely detected from the cycling 3T3-L1 cells without contact inhibition under the same inducing conditions (Fig 1B)
In order to determine whether the adipocyte differentiation is induced by cell cycle arrest, we analyzed the differentiation of 3T3-L1 cells with serum starved conditions, the results showed that adipocytes were not detected in serum starved conditions (Fig 1B)
Summary
The prevalence of overweight and obesity in developed and developing countries has greatly increased the risk of insulin resistance and type 2 diabetes mellitus. Clonal expansion and terminal differentiation of preadipocytes are required for generation of mature adipocytes [1]. These processes are controlled by a complex network of transcription factors, including peroxisome proliferator-activated receptor γ (PPARγ), CCAT/enhancer binding proteins, Krupple-like factors and sterol regulatory element-binding proteins, as well as extracellular hormones [2, 3]. Guo et al showed that adipocytes were barely detected from the population of the cycling 3T3-L1 cells without contact inhibition under inducing conditions [4], which indicated that CI stage is prerequisite for adipocyte differentiation.
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