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N-acetylcysteine inhibits kinase phosphorylation during 3T3-L1 adipocyte differentiation. | LitMetric

N-acetylcysteine inhibits kinase phosphorylation during 3T3-L1 adipocyte differentiation.

Redox Rep

a Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales , Universidad de Buenos Aires - IQUIBICEN, CONICET , Buenos Aires , Argentina.

Published: November 2017

AI Article Synopsis

Article Abstract

Objectives: Reports investigating the effects of antioxidants on obesity have provided contradictory results. We have previously demonstrated that treatment with the antioxidant N-acetylcysteine (NAC) inhibits cellular triglyceride (Tg) accumulation as well as total cellular monoamine oxidase A (MAOA) expression in 3T3-L1 mature adipocytes (Calzadilla et al., Redox Rep. 2013;210-218). Here we analyzed the role of NAC on adipogenic differentiation pathway.

Methods: Assays were conducted using 3T3-L1 preadipocytes (undifferentiated cells: CC), which are capable of differentiating into mature adipocytes (differentiated cells: DC). We studied the effects of different doses of NAC (0.01 or 1 mM) on DC, to evaluate cellular expression of phospho-JNK½ (pJNK½), phospho-ERK½ (pERK½) and, mitochondrial expression of citrate synthase, fumarate hydratase and MAOA.

Results: Following the differentiation of preadipocytes, an increase in the expression levels of pJNK½ and pERK½ was observed, together with mitotic clonal expansion (MCE). We found that both doses of NAC decreased the expression of pJNK½ and pERK½. Consistent with these results, NAC significantly inhibited MCE and modified the expression of different mitochondrial proteins.

Discussion: Our results suggested that NAC could inhibit Tg and mitochondrial protein expression by preventing both MCE and kinase phosphorylation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6837516PMC
http://dx.doi.org/10.1080/13510002.2016.1223267DOI Listing

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