N-acetylcysteine inhibits lipid accumulation in mouse embryonic adipocytes

Oxidative stress plays critical roles in the pathogenesis of diabetes, hypertension, and atherosclerosis; some authors reported that fat accumulation correlates to systemic oxidative stress in human and mice, but cellular redox environment effect on lipid accumulation is still unclear. In our labora...

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Autores principales: Martini, Claudia Noemí, Vila, María del Carmen, Calvo, Juan Carlos, Guerra, Liliana Noemí
Publicado: 2016
Materias:
MEF
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_22132317_v9_n_p39_Pieralisi
http://hdl.handle.net/20.500.12110/paper_22132317_v9_n_p39_Pieralisi
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spelling paper:paper_22132317_v9_n_p39_Pieralisi2023-06-08T16:35:17Z N-acetylcysteine inhibits lipid accumulation in mouse embryonic adipocytes Martini, Claudia Noemí Vila, María del Carmen Calvo, Juan Carlos Guerra, Liliana Noemí Adipogenesis Antioxidants Kinases Lipids MEF N-acetylcysteine acetylcysteine Janus kinase mitogen activated protein kinase phosphoERK phosphoJNK phosphoprotein triacylglycerol unclassified drug acetylcysteine phosphotransferase adipocyte adipogenesis animal cell animal tissue antioxidant activity Article cell count cell differentiation cell function cell level cell proliferation cell stress cell viability concentration response controlled study disease model drug cytotoxicity drug effect embryo enzyme phosphorylation lipid storage mitotic clonal expansion mouse nonhuman obesity priority journal procedures concerning cells protein expression protein lipid interaction signal transduction 3T3-L1 cell line adipocyte animal cytology drug effects fibroblast lipid metabolism mammalian embryo metabolism phosphorylation 3T3-L1 Cells Acetylcysteine Adipocytes Adipogenesis Animals Cell Differentiation Embryo, Mammalian Fibroblasts Lipid Metabolism Mice Phosphorylation Phosphotransferases Oxidative stress plays critical roles in the pathogenesis of diabetes, hypertension, and atherosclerosis; some authors reported that fat accumulation correlates to systemic oxidative stress in human and mice, but cellular redox environment effect on lipid accumulation is still unclear. In our laboratory we used mouse embryonic fibroblasts (undifferentiated cells: CC), which are capable of differentiating into mature adipocytes (differentiated cells: DC) and accumulate lipids, as obesity model. Here we analyzed the role of the well-known antioxidant and glutathione precursor N-acetylcysteine (NAC) in cellular MAPK modulation and lipid accumulation. We evaluated the effect of NAC on the adipogenic differentiation pathway using different doses: 0.01, 0.1, 1 and 5 mM; no toxic doses in these cells. A dose of 5 mM NAC [DCN-5] provoked a significant decrease in triglyceride accumulation (72±10 [DCN-5] vs 169±15 [DC], p<0.01), as well in Oil Red O stained neutral lipid content (120±2 [DCN-5] vs 139±12 [DC], p<0.01). Molecular mechanisms responsible for adipogenic differentiation involve increase of the expression of phosphoERK1/2 and phosphoJNK, 5 mM NAC treatment inhibited both pERK1/2 and pJNK protein levels. We also evaluated the mitotic clonal expansion (MCE) which takes place during adipogenesis and observed an increase in DC at a rate of 1.5 cells number compared to CC at day 2, whereas the highest doses of NAC significantly inhibited MCE. Our results suggest that NAC inhibits lipid accumulation and the MAPK phosphorylation in mouse embryonic fibroblasts during adipogenic differentiation and further contribute to probe the importance of cellular redox environment in adipogenesis. © 2016 The Authors. Fil:Martini, C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Vila, M.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Calvo, J.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Guerra, L.N. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2016 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_22132317_v9_n_p39_Pieralisi http://hdl.handle.net/20.500.12110/paper_22132317_v9_n_p39_Pieralisi
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Adipogenesis
Antioxidants
Kinases
Lipids
MEF
N-acetylcysteine
acetylcysteine
Janus kinase
mitogen activated protein kinase
phosphoERK
phosphoJNK
phosphoprotein
triacylglycerol
unclassified drug
acetylcysteine
phosphotransferase
adipocyte
adipogenesis
animal cell
animal tissue
antioxidant activity
Article
cell count
cell differentiation
cell function
cell level
cell proliferation
cell stress
cell viability
concentration response
controlled study
disease model
drug cytotoxicity
drug effect
embryo
enzyme phosphorylation
lipid storage
mitotic clonal expansion
mouse
nonhuman
obesity
priority journal
procedures concerning cells
protein expression
protein lipid interaction
signal transduction
3T3-L1 cell line
adipocyte
animal
cytology
drug effects
fibroblast
lipid metabolism
mammalian embryo
metabolism
phosphorylation
3T3-L1 Cells
Acetylcysteine
Adipocytes
Adipogenesis
Animals
Cell Differentiation
Embryo, Mammalian
Fibroblasts
Lipid Metabolism
Mice
Phosphorylation
Phosphotransferases
spellingShingle Adipogenesis
Antioxidants
Kinases
Lipids
MEF
N-acetylcysteine
acetylcysteine
Janus kinase
mitogen activated protein kinase
phosphoERK
phosphoJNK
phosphoprotein
triacylglycerol
unclassified drug
acetylcysteine
phosphotransferase
adipocyte
adipogenesis
animal cell
animal tissue
antioxidant activity
Article
cell count
cell differentiation
cell function
cell level
cell proliferation
cell stress
cell viability
concentration response
controlled study
disease model
drug cytotoxicity
drug effect
embryo
enzyme phosphorylation
lipid storage
mitotic clonal expansion
mouse
nonhuman
obesity
priority journal
procedures concerning cells
protein expression
protein lipid interaction
signal transduction
3T3-L1 cell line
adipocyte
animal
cytology
drug effects
fibroblast
lipid metabolism
mammalian embryo
metabolism
phosphorylation
3T3-L1 Cells
Acetylcysteine
Adipocytes
Adipogenesis
Animals
Cell Differentiation
Embryo, Mammalian
Fibroblasts
Lipid Metabolism
Mice
Phosphorylation
Phosphotransferases
Martini, Claudia Noemí
Vila, María del Carmen
Calvo, Juan Carlos
Guerra, Liliana Noemí
N-acetylcysteine inhibits lipid accumulation in mouse embryonic adipocytes
topic_facet Adipogenesis
Antioxidants
Kinases
Lipids
MEF
N-acetylcysteine
acetylcysteine
Janus kinase
mitogen activated protein kinase
phosphoERK
phosphoJNK
phosphoprotein
triacylglycerol
unclassified drug
acetylcysteine
phosphotransferase
adipocyte
adipogenesis
animal cell
animal tissue
antioxidant activity
Article
cell count
cell differentiation
cell function
cell level
cell proliferation
cell stress
cell viability
concentration response
controlled study
disease model
drug cytotoxicity
drug effect
embryo
enzyme phosphorylation
lipid storage
mitotic clonal expansion
mouse
nonhuman
obesity
priority journal
procedures concerning cells
protein expression
protein lipid interaction
signal transduction
3T3-L1 cell line
adipocyte
animal
cytology
drug effects
fibroblast
lipid metabolism
mammalian embryo
metabolism
phosphorylation
3T3-L1 Cells
Acetylcysteine
Adipocytes
Adipogenesis
Animals
Cell Differentiation
Embryo, Mammalian
Fibroblasts
Lipid Metabolism
Mice
Phosphorylation
Phosphotransferases
description Oxidative stress plays critical roles in the pathogenesis of diabetes, hypertension, and atherosclerosis; some authors reported that fat accumulation correlates to systemic oxidative stress in human and mice, but cellular redox environment effect on lipid accumulation is still unclear. In our laboratory we used mouse embryonic fibroblasts (undifferentiated cells: CC), which are capable of differentiating into mature adipocytes (differentiated cells: DC) and accumulate lipids, as obesity model. Here we analyzed the role of the well-known antioxidant and glutathione precursor N-acetylcysteine (NAC) in cellular MAPK modulation and lipid accumulation. We evaluated the effect of NAC on the adipogenic differentiation pathway using different doses: 0.01, 0.1, 1 and 5 mM; no toxic doses in these cells. A dose of 5 mM NAC [DCN-5] provoked a significant decrease in triglyceride accumulation (72±10 [DCN-5] vs 169±15 [DC], p<0.01), as well in Oil Red O stained neutral lipid content (120±2 [DCN-5] vs 139±12 [DC], p<0.01). Molecular mechanisms responsible for adipogenic differentiation involve increase of the expression of phosphoERK1/2 and phosphoJNK, 5 mM NAC treatment inhibited both pERK1/2 and pJNK protein levels. We also evaluated the mitotic clonal expansion (MCE) which takes place during adipogenesis and observed an increase in DC at a rate of 1.5 cells number compared to CC at day 2, whereas the highest doses of NAC significantly inhibited MCE. Our results suggest that NAC inhibits lipid accumulation and the MAPK phosphorylation in mouse embryonic fibroblasts during adipogenic differentiation and further contribute to probe the importance of cellular redox environment in adipogenesis. © 2016 The Authors.
author Martini, Claudia Noemí
Vila, María del Carmen
Calvo, Juan Carlos
Guerra, Liliana Noemí
author_facet Martini, Claudia Noemí
Vila, María del Carmen
Calvo, Juan Carlos
Guerra, Liliana Noemí
author_sort Martini, Claudia Noemí
title N-acetylcysteine inhibits lipid accumulation in mouse embryonic adipocytes
title_short N-acetylcysteine inhibits lipid accumulation in mouse embryonic adipocytes
title_full N-acetylcysteine inhibits lipid accumulation in mouse embryonic adipocytes
title_fullStr N-acetylcysteine inhibits lipid accumulation in mouse embryonic adipocytes
title_full_unstemmed N-acetylcysteine inhibits lipid accumulation in mouse embryonic adipocytes
title_sort n-acetylcysteine inhibits lipid accumulation in mouse embryonic adipocytes
publishDate 2016
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_22132317_v9_n_p39_Pieralisi
http://hdl.handle.net/20.500.12110/paper_22132317_v9_n_p39_Pieralisi
work_keys_str_mv AT martiniclaudianoemi nacetylcysteineinhibitslipidaccumulationinmouseembryonicadipocytes
AT vilamariadelcarmen nacetylcysteineinhibitslipidaccumulationinmouseembryonicadipocytes
AT calvojuancarlos nacetylcysteineinhibitslipidaccumulationinmouseembryonicadipocytes
AT guerraliliananoemi nacetylcysteineinhibitslipidaccumulationinmouseembryonicadipocytes
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