Bone marrow p16INK4a-deficiency does not modulate obesity, glucose homeostasis or atherosclerosis development.

<h4>Objective</h4>A genomic region near the CDKN2A locus, encoding p16(INK4a), has been associated to type 2 diabetes and atherosclerotic vascular disease, conditions in which inflammation plays an important role. Recently, we found that deficiency of p16(INK4a) results in decreased infl...

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Autores principales: Kristiaan Wouters, Céline Cudejko, Marion J J Gijbels, Lucia Fuentes, Kadiombo Bantubungi, Jonathan Vanhoutte, Rebecca Dièvart, Charlotte Paquet, Emmanuel Bouchaert, Sarah Anissa Hannou, Florence Gizard, Anne Tailleux, Menno P J de Winther, Bart Staels, Réjane Paumelle
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Publicado: Public Library of Science (PLoS) 2012
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spelling oai:doaj.org-article:f1eb7ebaa8ee485b9bc67339bc01578d2021-11-18T07:26:07ZBone marrow p16INK4a-deficiency does not modulate obesity, glucose homeostasis or atherosclerosis development.1932-620310.1371/journal.pone.0032440https://doaj.org/article/f1eb7ebaa8ee485b9bc67339bc01578d2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22403661/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Objective</h4>A genomic region near the CDKN2A locus, encoding p16(INK4a), has been associated to type 2 diabetes and atherosclerotic vascular disease, conditions in which inflammation plays an important role. Recently, we found that deficiency of p16(INK4a) results in decreased inflammatory signaling in murine macrophages and that p16(INK4a) influences the phenotype of human adipose tissue macrophages. Therefore, we investigated the influence of immune cell p16(INK4a) on glucose tolerance and atherosclerosis in mice.<h4>Methods and results</h4>Bone marrow p16(INK4a)-deficiency in C57Bl6 mice did not influence high fat diet-induced obesity nor plasma glucose and lipid levels. Glucose tolerance tests showed no alterations in high fat diet-induced glucose intolerance. While bone marrow p16(INK4a)-deficiency did not affect the gene expression profile of adipose tissue, hepatic expression of the alternative markers Chi3l3, Mgl2 and IL10 was increased and the induction of pro-inflammatory Nos2 was restrained on the high fat diet. Bone marrow p16(INK4a)-deficiency in low density lipoprotein receptor-deficient mice did not affect western diet-induced atherosclerotic plaque size or morphology. In line, plasma lipid levels remained unaffected and p16(INK4a)-deficient macrophages displayed equal cholesterol uptake and efflux compared to wild type macrophages.<h4>Conclusion</h4>Bone marrow p16(INK4a)-deficiency does not affect plasma lipids, obesity, glucose tolerance or atherosclerosis in mice.Kristiaan WoutersCéline CudejkoMarion J J GijbelsLucia FuentesKadiombo BantubungiJonathan VanhoutteRebecca DièvartCharlotte PaquetEmmanuel BouchaertSarah Anissa HannouFlorence GizardAnne TailleuxMenno P J de WintherBart StaelsRéjane PaumellePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 3, p e32440 (2012)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Kristiaan Wouters
Céline Cudejko
Marion J J Gijbels
Lucia Fuentes
Kadiombo Bantubungi
Jonathan Vanhoutte
Rebecca Dièvart
Charlotte Paquet
Emmanuel Bouchaert
Sarah Anissa Hannou
Florence Gizard
Anne Tailleux
Menno P J de Winther
Bart Staels
Réjane Paumelle
Bone marrow p16INK4a-deficiency does not modulate obesity, glucose homeostasis or atherosclerosis development.
description <h4>Objective</h4>A genomic region near the CDKN2A locus, encoding p16(INK4a), has been associated to type 2 diabetes and atherosclerotic vascular disease, conditions in which inflammation plays an important role. Recently, we found that deficiency of p16(INK4a) results in decreased inflammatory signaling in murine macrophages and that p16(INK4a) influences the phenotype of human adipose tissue macrophages. Therefore, we investigated the influence of immune cell p16(INK4a) on glucose tolerance and atherosclerosis in mice.<h4>Methods and results</h4>Bone marrow p16(INK4a)-deficiency in C57Bl6 mice did not influence high fat diet-induced obesity nor plasma glucose and lipid levels. Glucose tolerance tests showed no alterations in high fat diet-induced glucose intolerance. While bone marrow p16(INK4a)-deficiency did not affect the gene expression profile of adipose tissue, hepatic expression of the alternative markers Chi3l3, Mgl2 and IL10 was increased and the induction of pro-inflammatory Nos2 was restrained on the high fat diet. Bone marrow p16(INK4a)-deficiency in low density lipoprotein receptor-deficient mice did not affect western diet-induced atherosclerotic plaque size or morphology. In line, plasma lipid levels remained unaffected and p16(INK4a)-deficient macrophages displayed equal cholesterol uptake and efflux compared to wild type macrophages.<h4>Conclusion</h4>Bone marrow p16(INK4a)-deficiency does not affect plasma lipids, obesity, glucose tolerance or atherosclerosis in mice.
format article
author Kristiaan Wouters
Céline Cudejko
Marion J J Gijbels
Lucia Fuentes
Kadiombo Bantubungi
Jonathan Vanhoutte
Rebecca Dièvart
Charlotte Paquet
Emmanuel Bouchaert
Sarah Anissa Hannou
Florence Gizard
Anne Tailleux
Menno P J de Winther
Bart Staels
Réjane Paumelle
author_facet Kristiaan Wouters
Céline Cudejko
Marion J J Gijbels
Lucia Fuentes
Kadiombo Bantubungi
Jonathan Vanhoutte
Rebecca Dièvart
Charlotte Paquet
Emmanuel Bouchaert
Sarah Anissa Hannou
Florence Gizard
Anne Tailleux
Menno P J de Winther
Bart Staels
Réjane Paumelle
author_sort Kristiaan Wouters
title Bone marrow p16INK4a-deficiency does not modulate obesity, glucose homeostasis or atherosclerosis development.
title_short Bone marrow p16INK4a-deficiency does not modulate obesity, glucose homeostasis or atherosclerosis development.
title_full Bone marrow p16INK4a-deficiency does not modulate obesity, glucose homeostasis or atherosclerosis development.
title_fullStr Bone marrow p16INK4a-deficiency does not modulate obesity, glucose homeostasis or atherosclerosis development.
title_full_unstemmed Bone marrow p16INK4a-deficiency does not modulate obesity, glucose homeostasis or atherosclerosis development.
title_sort bone marrow p16ink4a-deficiency does not modulate obesity, glucose homeostasis or atherosclerosis development.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/f1eb7ebaa8ee485b9bc67339bc01578d
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