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Advanced oxidation protein products inhibit differentiation and activate inflammation in 3T3-L1 preadipocytes
Qiu Gen Zhou1, Xin Peng, Li Li Hu
1Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Abstract:
Accumulation of advanced oxidation protein products (AOPPs) is prevalent in metabolic syndromes, a condition with impaired preadipocytes differentiation. In the present study, we tested the hypothesis that AOPPs disturb preadipocyte differentiation. Exposure of 3T3-L1 preadipocytes to increased levels of AOPPs inhibited accumulation of intracellular triglyceride and decreased the expression of the essential markers of matured adipocytes, such as adipocyte fatty-acid-binding protein (aP2), CAAT/enhancer-binding protein (C/EBP)-alpha, and peroxisome proliferator-activated receptor (PPAR)-gamma, in response to standard adipogenic induction. Inhibitory effects of AOPPs on preadipocytes differentiation was time sensitive, which occurred at the early stage of differentiation. In the presence of AOPPs, induction of preadipocytes differentiation resulted in upregulated expression of C/EBP homologous protein (CHOP) and CUG-Triplet repeat-binding protein (CUGBP), two important inhibitors of preadipocytes differentiation. In addition, treatment with AOPPs increased abundance of C/EBP-beta-liver enriched inhibitory protein (C/EBP-beta-LIP), a truncated C/EBP-beta isoform without adipogenic activity. Moreover, AOPPs-treated preadipocytes expressed a macrophage marker F4/80 and overexpressed tumor necrosis factor-alpha and interleukin-6 via nuclear factor-kappaB (NF-kappaB)-dependent pathway. However, blocking inflammation with NF-kappaB inhibitor failed to improve AOPPs-induced inhibition of preadipocytes differentiation. These data suggest that accumulation of AOPPs may inhibit differentiation of preadipocytes and activate inflammation in these cells. This information might have implication for understanding the impairment of preadipocytes differentiation and fat inflammation seen in metabolic syndrome.
Insights
Advanced oxidation protein products (AOPPs) hinder preadipocyte differentiation, a key process in metabolic syndromes. AOPPs inhibit fat cell formation and promote inflammation, contributing to metabolic dysfunction.
Area of Science:
- Cell Biology
- Metabolic Syndrome Research
- Biochemistry
Background:
- Metabolic syndromes are characterized by impaired preadipocyte differentiation.
- Accumulation of advanced oxidation protein products (AOPPs) is a common feature of metabolic syndromes.
Purpose of the Study:
- To investigate the effect of AOPPs on preadipocyte differentiation.
- To elucidate the molecular mechanisms by which AOPPs influence adipogenesis and inflammation.
Main Methods:
- Exposure of 3T3-L1 preadipocytes to varying levels of AOPPs.
- Analysis of intracellular triglyceride accumulation and expression of adipocyte differentiation markers (aP2, C/EBP-alpha, PPAR-gamma).
- Assessment of inflammatory markers (F4/80, TNF-alpha, IL-6) and signaling pathways (NF-kappaB).
Main Results:
- AOPPs significantly inhibited preadipocyte differentiation, reducing triglyceride accumulation and key adipocyte marker expression.
- AOPPs upregulated differentiation inhibitors (CHOP, CUGBP) and a non-adipogenic C/EBP-beta isoform (C/EBP-beta-LIP).
- AOPPs induced macrophage marker expression and pro-inflammatory cytokine release via the NF-kappaB pathway, though NF-kappaB inhibition did not rescue differentiation.
Conclusions:
- Accumulation of AOPPs impairs preadipocyte differentiation by interfering with early differentiation stages.
- AOPPs promote inflammation in preadipocytes through NF-kappaB-dependent pathways.
- These findings offer insights into the role of AOPPs in metabolic syndrome-associated adipocyte dysfunction and inflammation.
