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Suppression of preadipocyte determination by SOX4 limits white adipocyte hyperplasia in obesity
Ting He1, Shuai Wang1, Shengnan Li1,2
1State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network and Engineering Research Center of Molecular Diagnostics of The Ministry of Education, School of Life Sciences, Xiamen University, Xiamen, Fujian 361100, China.
Abstract:
Preadipocyte determination expanding the pool of preadipocytes is a vital process in adipocyte hyperplasia, but the molecular mechanisms underlying this process are yet to be elucidated. Herein, SRY-related HMG box transcription factor 4 (SOX4) was identified as a critical target in response to BMP4- and TGFβ-regulated preadipocyte determination. SOX4 deficiency is sufficient to promote preadipocyte determination in mesenchymal stem cells (MSCs) and acquisition of preadipocyte properties in nonadipogenic lineages, while its overexpression impairs the adipogenic capacity of preadipocytes and converts them into nonadipogenic lineages. Mechanism studies indicated that SOX4 activates and cooperates with LEF1 to retain the nuclear localization of β-catenin, thus mediating the crosstalk between TGFβ/BMP4 signaling pathway and Wnt signaling pathway to regulate the preadipocyte determination. In vivo studies demonstrated that SOX4 promotes the adipogenic-nonadipogenic conversion and suppresses the adipocyte hyperplasia. Together, our findings highlight the importance of SOX4 in regulating the adipocyte hyperplasia in obesity.
Insights
SRY-related HMG box transcription factor 4 (SOX4) regulates the expansion of preadipocytes. SOX4 deficiency promotes preadipocyte determination, while its overexpression impairs adipogenesis, highlighting its role in obesity.
Area of Science:
- Cell Biology
- Molecular Biology
- Endocrinology
Background:
- Preadipocyte determination is crucial for increasing the number of adipocytes (adipocyte hyperplasia).
- The molecular mechanisms controlling preadipocyte determination remain largely unknown.
- Understanding these mechanisms is vital for addressing obesity.
Purpose of the Study:
- To elucidate the molecular mechanisms of preadipocyte determination.
- To identify key regulators involved in adipocyte hyperplasia.
- To investigate the role of SOX4 in adipogenesis and obesity.
Main Methods:
- Investigated the role of SOX4 in preadipocyte determination using mesenchymal stem cells (MSCs).
- Utilized overexpression and deficiency models of SOX4.
- Examined the interaction of SOX4 with LEF1 and β-catenin.
- Conducted in vivo studies to assess SOX4 function in adipocyte hyperplasia.
Main Results:
- SOX4 deficiency promotes preadipocyte determination in MSCs and acquisition of adipocyte properties in non-adipogenic cells.
- SOX4 overexpression impairs adipogenic capacity and promotes conversion to non-adipogenic lineages.
- SOX4, along with LEF1, retains nuclear β-catenin, linking TGFβ/BMP4 and Wnt signaling pathways.
- In vivo studies confirmed SOX4 promotes adipogenic-non-adipogenic conversion and suppresses adipocyte hyperplasia.
Conclusions:
- SOX4 is a critical regulator of preadipocyte determination and adipocyte hyperplasia.
- SOX4 mediates crosstalk between TGFβ/BMP4 and Wnt signaling pathways.
- SOX4 plays a significant role in adipocyte hyperplasia, a key factor in obesity.
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