Abstract
Sestrin-3, together with the other two members Sestrin-1 and Sestrin-2, belongs to the Sestrin family. The Sestrin protein family has been demonstrated to be involved in antioxidative, metabolic homeostasis, and even the development of nonalcoholic steatohepatitis (NASH). However, the adipogenic regulatory role of SESN3 in adipogenesis still needs to be further explored. In this study, we demonstrated SESN3 inhibited porcine pre-adipocyte proliferation, thus suppressing its adipogenesis. Meanwhile, SESN3 has been demonstrated to inhibit Smad3 thus protecting against NASH. Further, for our previous study, we found mmu-miR-124 involved in 3T3-L1 cell adipogenesis regulation. In this study, we also identified that ssc-miR-124 inhibited porcine pre-adipocyte proliferation, thus suppressing its adipogenesis, and the SMAD3 was an inhibitor of ssc-miR-124 by binding to its promoter. Furthermore, the ssc-miR-124 targeted porcine C/EBPα and GR and thus inhibited pre-adipocyte adipogenesis. In conclusion, SESN3 inhibited SMAD3, thus improving ssc-miR124, and then suppressed C/EBPα and GR to regulate pre-adipocytes adipogenesis.
Highlights
Katarzyna Piórkowska and Overweight and obesity lead to a batch of diseases including but not limited to metabolic disease, hypertension, cardiovascular disease, and type II diabetes (T2D), which becomes one of the major threats to human health [1,2]
We constructed the pcDNA3.1-Sesn3-CDS vector to explore its proliferative role in pre-adipocytes, transfected them into pre-adipocytes for 48 h and detected their proliferative efficiency by EdU incubation and Cell Counting Kit-8 (CCK-8) detection
CCK-8 detection resulted in further identified SESN3-inhibited pre-adipocyte proliferation (Figure 1C)
Summary
Katarzyna Piórkowska and Overweight and obesity lead to a batch of diseases including but not limited to metabolic disease, hypertension, cardiovascular disease, and type II diabetes (T2D), which becomes one of the major threats to human health [1,2]. As a basic unit of adipose tissue, adipocyte differentiation and proliferation lead to adipose tissue expansion, and excessive adipose tissue cause obesity-related metabolic syndromes. Adipocytes are emerging as a significant target in the treatment of obesity-related metabolic syndromes in the clinical setting [3]. The molecular mechanisms of adipocyte differentiation and proliferation are of significant and escalating biomedical interest. According to the classical extensive consensus on adipogenesis, hundreds of factors and genes involve enormous and complicated interaction networks to control this progress.
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