Adipocyte
·
2021
·
IF 4.534
Jingwei Zhang,Wei Wang,Ninghan Feng,Xuan Jiang,Shenglong Zhu,Yong Q Chen
Obesity and associated complications are becoming a pandemic. Inhibiting adipogenesis is an important intervention for the treatment of obesity. Despite intensive investigations, numerous mechanistic aspects of adipogenesis remain unclear, and many potential therapeutic targets have yet to be discovered. Transcriptomics and lipidomics approaches were used to explore the functional genes regulating adipogenic differentiation and the potential mechanism in OP9 cells and adipose-derived stem cells. In this study, we found that NADH:ubiquinone oxidoreductase subunit A6 (Ndufa6) participates in the regulation of adipogenic differentiation. Furthermore, we show that the effect of Ndufa6 is mediated through stearoyl-CoA desaturase 1 (Scd1) and demonstrate the inhibitory effect of a SCD1 inhibitor on adipogenesis. Our study broadens the understanding of adipogenic differentiation and offers NDUFA6-SCD1 as a potential therapeutic target for the treatment of obesity.
研究领域:
分子生物学
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细胞生物学
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代谢
·
肥胖研究
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DOI
PubMed
高影响因子
CELLULAR & MOLECULAR BIOLOGY LETTERS
·
2022
·Vol. 27
·期 1
·1-13
·
IF 8.702
Zhu Shenglong,Wang Wei,Zhang Jingwei,Ji Siyu,Jing Zhe,Chen Yong Q.
Background A comprehensive understanding of the molecular mechanisms of adipogenesis is a critically important strategy for identifying new targets for obesity intervention. Methods Transcriptomic and lipidomic approaches were used to explore the functional genes regulating adipogenic differentiation and their potential mechanism of action in OP9 cells and adipose-derived stem cells. Oil Red O staining was used to detect oil droplets in adipocytes. Results RNA sequencing (RNA-seq) showed that Slc25a5 expression was significantly upregulated in adipogenic differentiation. Depletion of Slc25a5 led to the suppressed expression of adipogenesis-related genes, reduced the accumulation of triglycerides, and inhibited PPARγ protein expression. Moreover, the knockdown of Slc25a5 resulted in significant reduction of oxidative phosphorylation (OXPHOS) protein expression (ATP5A1, CQCRC2, and MTCO1) and ATP production. The RNA-seq and real-time quantitative polymerase chain reaction (RT–qPCR) results suggested that adipogenic differentiation is possibly mediated by ERK1/2 phosphorylation, and this hypothesis was confirmed by intervention with PD98059 (an ERK 1/2 inhibitor). Conclusions This study indicates that Slc25a5 inhibits adipogenesis and might be a new therapeutic target for the treatment of obesity.
研究领域:
分子生物学
·
细胞生物学
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肥胖研究
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY
·
2022
·Vol. 78
·期 2
·377-388
·
IF 5.08
Zhu Shenglong,Zhang Jingwei,Wang Wei,Jiang Xuan,Chen Yong Q.
Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease with an increasing global prevalence associated with tremendous clinical, economic, and health-related quality-of-life burden. Currently, no effective pharmacological therapy is available for NAFLD. Adipogenesis process is accompanied by fat synthesis which may participate in the occurrence and development of NAFLD. Despite intensive investigations, numerous mechanistic aspects of adipogenesis remain unclear and many potential therapeutic targets are yet to be discovered. In this study, the transcriptomics and lipidomics approaches were used to explore the functional genes regulating adipogenesis and the potential mechanism in OP9 cells and adipose-derived stem cells. We find that NADH:ubiquinone oxidoreductase subunit b9 ( Ndufb9 ) is up-regulated in adipogenesis ( p < 0.001), and silencing Ndufb9 (83% silencing efficiency) inhibits adipogenesis. The effect of Ndufb9 is mediated through stearoyl-CoA desaturase 1 ( Scd1 ). Aramchol, a SCD1 inhibitor, significantly blocks adipogenesis (markedly TG decrease, p < 0.001). Our study broadens the understanding of the role of Ndufb9 in adipogenesis and provides a new target for the treatment of NAFLD.
研究领域:
分子生物学
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细胞生物学
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药理学
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代谢性疾病
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产品关联
DOI
PubMed
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2024
·
IF 2.5
Yao Jiang,Wei Wang,Hui Wang,Xiaoru Zhang,Yuling Kong,Yong Q. Chen,Shenglong Zhu
Aberrant adipogenic differentiation is strongly associated with obesity and related metabolic diseases. Elucidating the key factors driving adipogenesis is an effective strategy for identifying novel therapeutic targets for treating metabolic diseases represented by obesity. In this study, transcriptomic techniques were employed to investigate the functional genes that regulate adipogenic differentiation in OP9 cells and 3T3-L1 cells. The findings indicated a notable upregulation of Acsl1 expression throughout the adipogenic differentiation process. Knocking down Acsl1 led to a decrease in the expression of genes associated with adipogenesis and a reduction in triglyceride accumulation. Additionally, Acsl1 overexpression promoted adipocyte differentiation and adipose-specific overexpression of Acsl1 markedly aggravated steatosis induced by a high-fat diet. Mechanistically, Cyp2f2, Dusp23 and Gstm2 are the crucial genes implicated in Acsl1-induced adipogenic differentiation. The findings of this study indicate that Acsl1 promotes adipogenesis and could serve as a potential therapeutic target for treating obesity and related metabolic disorders.
研究领域:
分子生物学
·
细胞生物学
·
代谢
·
肥胖研究
✓ 已验证
DOI
高影响因子
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