Transcription Factor 21 Promotes Chicken Adipocyte Differentiation at Least in Part via Activating MAPK/JNK Signaling

Abstract

The molecular mechanisms of transcription factor 21 (TCF21) in regulating chicken adipogenesis remain unclear. Thus, the current study was designed to investigate the signaling pathway mediating the effect of TCF21 on chicken adipogenesis. Immortalized chicken preadipocytes cell line (ICP), a preadipocyte cell line stably overexpressing TCF21 (LV-TCF21) and a control preadipocyte cell line (LV-control) were used in the current study. We found that the phosphorylation of c-Jun N-terminal kinases (JNK) was significantly elevated in LV-TCF21 compared to LV-control. After treating ICP cells with a JNK inhibitor SP600125, the differentiation of ICP was inhibited, as evidenced by decreased accumulation of lipid droplets and reduced expression of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding protein α (C/EBPα), adipocyte fatty acid binding protein (A-FABP), and lipoprotein lipase (LPL). Moreover, we found that the inhibition of JNK by SP600125 remarkably impaired the ability of TCF21 to drive adipogenesis. Taken together, our results suggest that TCF21 promotes the differentiation of adipocytes at least in part via activating MAPK/JNK pathway.

Polymorphism rs2327430 in TCF21 predicts the risk and prognosis of gastric cancer by affecting the binding between TFAP2A and TCF21

“…The mechanism by which TCF21 affects malignant behaviors in GC is also noteworthy. TCF21 has been reported to influence multiple pathways, including the PI3K-AKT pathway and MAPK pathway [ 48 , 49 ]. However, further validation is needed to identify the direct target genes of TCF21 that regulate these downstream signaling pathways.…”

KRAS Affects the Lipid Composition by Regulating Mitochondrial Functions and MAPK Activation in Bovine Mammary Epithelial Cells

“…Previous studies have shown that microtubule affinity regulating kinase 4 can also promote lipid formation by inhibiting p38 and activating JNK1, and JNK activation promotes mesenchymal stem cell adipogenic differentiation [ 78 ]; these results seem to suggest that JNK plays opposite roles to ERK and p38 in adipogenesis. In this study, the differential expression of related genes also demonstrated that KRAS inhibition can activate the JNK pathway, thus promoting lipid formation by regulating PPARG and FABP4 [ 79 ]. After KRAS inhibition, the phosphorylation level of JNK increased, while the levels of ERK and p38 decreased at the same time, which suggests that KRAS plays important roles in lipid accumulation in MAC-T cells.…”