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.
Highlights
In the poultry industry, excessive fat deposition in broiler chicken is not wanted by most customers, because many metabolic diseases like coronary heart disease and arteriosclerosis are strongly related to increased dietary intake of cholesterol [1]
We utilized Immortalized chicken preadipocytes cell line (ICP) established by infecting primary chicken preadipocytes with the recombinant retroviruses expressing chicken telomerase reverse transcriptase and telomerase RNA [16], LV-transcription factor 21 (TCF21) established by infecting ICP with the recombinant lentivirus expressing chicken TCF21, and LV-control established by infecting ICP with the control lentivirus [15]
It has been reported that TCF21 is not expressed in brown preadipocytes and is instead specific to white preadipocytes TCF21 [18], and compared with brown adipose tissues, the expression of TCF21 is more abundant in white adipose tissues [19]
Summary
Excessive fat deposition in broiler chicken is not wanted by most customers, because many metabolic diseases like coronary heart disease and arteriosclerosis are strongly related to increased dietary intake of cholesterol [1]. Increased dietary cholesterol intake from fat may lead to increased serum cholesterol levels and further increased risks of metabolic diseases [2,3]. Excessive fat deposition hinders processing and leads to significant reductions in feed efficiency and carcass yield, incurring economic losses for poultry producers and processors [4,5]. Excessive fat deposition in chicken has increased the incidence of metabolic disorders, such as pulmonary hypertension syndrome, sudden death, fatty liver disease [6–8], and reduced reproductive performance, such as less sperm concentration, more sperm with abnormal morphology, and less egg production [9]. To facilitate therapeutic prevention or treatment of obesity, it is of great significance to get a deeper understanding of the molecular mechanisms involved in adipogenesis
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