ALDH1A1 Inhibits Chicken Preadipocytes' Proliferation and Differentiation via the PPAR gamma Pathway In Vitro and In Vivo

文献类型： 外文期刊

第一作者： Zhang, Jing

作者： Zhang, Jing;Cai, Bolin;Ma, Manting;Luo, Wei;Zhang, Zipeng;Zhang, Xiquan;Nie, Qinghua;Zhang, Jing;Cai, Bolin;Ma, Manting;Luo, Wei;Zhang, Zipeng;Zhang, Xiquan;Nie, Qinghua;Zhang, Jing;Cai, Bolin;Ma, Manting;Luo, Wei;Zhang, Zipeng;Zhang, Xiquan;Nie, Qinghua;Zhang, Jing;Cai, Bolin;Ma, Manting;Luo, Wei;Zhang, Zipeng;Zhang, Xiquan;Nie, Qinghua

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关键词： ALDH1A1; preadipocytes; proliferation; differentiation; adipogenesis; PPAR gamma pathway; chicken

期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：5.923； 五年影响因子：6.132 ）

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年卷期： 2020 年 21 卷 9 期

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收录情况： SCI

摘要： ALDH1A1 (aldehyde dehydrogenase 1A1) is a crucial protein in retinoids' metabolism, and the lack of ALDH1A1 inhibits the fat deposition in mice. However, whether ALDH1A1 has a similar effect on chickens' fat-depot is still unknown. In this study, we investigate the role of ALDH1A1 in chickens' adipogenesis. The immortalized chicken preadipocyte 1 (ICP1) cell line and chicken primary preadipocytes isolated from abdominal fat were used to perform a series of experiments in vitro to elucidate the effects of ALDH1A1. In addition, lentivirus was used to verify the results of cell experiments in vivo. The data showed that overexpression of ALDH1A1 significantly weakened the proliferation of preadipocytes and suppressed the differentiation of preadipocytes through the PPAR gamma pathway, and the knockdown experiments had the opposite results. Moreover, chickens injected with overexpression lentivirus had higher abdominal fat percentage, a bigger size of lipid droplets, and higher triglyceride content in abdominal fat, and chickens injected with interfering lentivirus had the opposite situation. We proved that ALDH1A1 not only inhibited the proliferation and differentiation of chickens' preadipocytes in vitro, but also inhibited the fat-depot of chickens in vivo, which was completely opposite the function of ALDH1A1 in mice, indicating that ALDH1A1 may have a different mechanism that is still unknown.

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