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Title:
Downregulation of the tumour suppressor p16INK4A contributes to the polarisation of human macrophages toward an adipose tissue macrophage (ATM)-like phenotype | Diabetologia
Description:
Aims/hypothesis Human adipose tissue macrophages (ATMs) display an alternatively activated (M2) phenotype, but are still able to produce excessive inflammatory mediators. However, the processes driving this particular ATM phenotype are not understood. Genome-wide association studies associated the CDKN2A locus, encoding the tumour suppressor p16INK4A, with the development of type 2 diabetes. In the present study, p16INK4A levels in human ATMs and the role of p16INK4A in acquiring the ATM phenotype were assessed. Methods Gene expression of p16 INK4A in ATMs was analysed and compared with that in monocyte-derived macrophages (MDMs) from obese patients or with macrophages from human atherosclerotic plaques (AMs). Additionally, p16INK4A levels were studied during macrophage differentiation and polarisation of monocytes isolated from healthy donors. The role of p16INK4A in MDMs from healthy donors was investigated by small interfering (si)RNA-mediated silencing or adenovirus-mediated overproduction of p16INK4A. Results Compared with MDMs and AMs, ATMs from obese patients expressed lower levels of p16 INK4A . In vitro, IL-4-induced M2 polarisation resulted in lower p16INK4A protein levels after differentiation of monocytes from healthy donors in macrophages. Silencing of p16INK4A in MDMs mediated by siRNA increased the expression of M2 marker genes and enhanced the response to lipopolysaccharide (LPS), to give a phenotype resembling that of ATM. By contrast, adenovirus-mediated overproduction of p16INK4A in MDMs diminished M2 marker gene expression and the response to LPS. Western blot analysis revealed that p16INK4A overproduction inhibits LPS- and palmitate-induced Toll-like receptor 4 (TLR4)–nuclear factor of κ light polypeptide gene enhancer in B cells (NF-κB) signalling. Conclusions/interpretation These results show that p16INK4A inhibits the acquisition of the ATM phenotype. The age-related increase in p16INK4A level may thus influence normal ATM function and contribute to type 2 diabetes risk.
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Keywords {🔍}
pinka, macrophages, levels, human, article, mdms, atms, google, scholar, pubmed, cas, phenotype, expression, macrophage, inka, fig, cell, france, lps, polarisation, adipose, tissue, cells, inflammatory, atm, protein, monocytes, nfκb, lille, data, activation, type, diabetes, differentiation, obese, overproduction, signalling, obesity, control, fuentes, genes, response, shown, mrna, tlr, analysis, wouters, role, gene, compared,
Topics {✒️}
genome-wide association studies induce anti-proliferative responses haptoglobin-haemoglobin scavenger receptor cd68+ macrophage-rich areas peroxisome proliferator-activated receptor stem-cell ageing modified hematopoietic cell-specific deletion pro-inflammatory phenotype found ikk-beta links inflammation receptor-mediated immune responses /cyclin-dependent kinase 4 high-fat-fed mice obesity-induced adipocyte hypertrophy mature monocyte-derived macrophages adenovirus-mediated gene transfer adipose tissue macrophage universitaire de lille lps-induced tnf secretion centre hospitalier régionale o'neill la human atherosclerotic plaques abdominal adipose tissue molecular mechanisms determining obesity-induced insulin resistance cell cycle inhibitor lps-induced m1 macrophages lps-induced inflammatory response privacy choices/manage cookies atlas biologique de ministerio de educación faculté de médecine electronic supplementary material pro-inflammatory mediators human carotid plaques macrophage-rich areas p16 ink4a overexpression atms increases significantly human atms involves altered inflammatory profile rneasy micro kit ink4/arf locus cell cycle exit cell cycle withdrawal phenotype article published anti-inflammatory properties enhance alternative polarisation age-dependent increase age-dependent decline m2 polarisation status pancreatic beta cells
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headline:Downregulation of the tumour suppressor p16INK4A contributes to the polarisation of human macrophages toward an adipose tissue macrophage (ATM)-like phenotype
description:Human adipose tissue macrophages (ATMs) display an alternatively activated (M2) phenotype, but are still able to produce excessive inflammatory mediators. However, the processes driving this particular ATM phenotype are not understood. Genome-wide association studies associated the CDKN2A locus, encoding the tumour suppressor p16INK4A, with the development of type 2 diabetes. In the present study, p16INK4A levels in human ATMs and the role of p16INK4A in acquiring the ATM phenotype were assessed. Gene expression of p16
INK4A
in ATMs was analysed and compared with that in monocyte-derived macrophages (MDMs) from obese patients or with macrophages from human atherosclerotic plaques (AMs). Additionally, p16INK4A levels were studied during macrophage differentiation and polarisation of monocytes isolated from healthy donors. The role of p16INK4A in MDMs from healthy donors was investigated by small interfering (si)RNA-mediated silencing or adenovirus-mediated overproduction of p16INK4A. Compared with MDMs and AMs, ATMs from obese patients expressed lower levels of p16
INK4A
. In vitro, IL-4-induced M2 polarisation resulted in lower p16INK4A protein levels after differentiation of monocytes from healthy donors in macrophages. Silencing of p16INK4A in MDMs mediated by siRNA increased the expression of M2 marker genes and enhanced the response to lipopolysaccharide (LPS), to give a phenotype resembling that of ATM. By contrast, adenovirus-mediated overproduction of p16INK4A in MDMs diminished M2 marker gene expression and the response to LPS. Western blot analysis revealed that p16INK4A overproduction inhibits LPS- and palmitate-induced Toll-like receptor 4 (TLR4)–nuclear factor of κ light polypeptide gene enhancer in B cells (NF-κB) signalling. These results show that p16INK4A inhibits the acquisition of the ATM phenotype. The age-related increase in p16INK4A level may thus influence normal ATM function and contribute to type 2 diabetes risk.
datePublished:2011-10-04T00:00:00Z
dateModified:2011-10-04T00:00:00Z
pageStart:3150
pageEnd:3156
sameAs:https://doi.org/10.1007/s00125-011-2324-0
keywords:
Adipose tissue macrophage
CDKN2A
Inflammation
Macrophage polarisation
Senescence
Type 2 diabetes
Internal Medicine
Metabolic Diseases
Human Physiology
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headline:Downregulation of the tumour suppressor p16INK4A contributes to the polarisation of human macrophages toward an adipose tissue macrophage (ATM)-like phenotype
description:Human adipose tissue macrophages (ATMs) display an alternatively activated (M2) phenotype, but are still able to produce excessive inflammatory mediators. However, the processes driving this particular ATM phenotype are not understood. Genome-wide association studies associated the CDKN2A locus, encoding the tumour suppressor p16INK4A, with the development of type 2 diabetes. In the present study, p16INK4A levels in human ATMs and the role of p16INK4A in acquiring the ATM phenotype were assessed. Gene expression of p16
INK4A
in ATMs was analysed and compared with that in monocyte-derived macrophages (MDMs) from obese patients or with macrophages from human atherosclerotic plaques (AMs). Additionally, p16INK4A levels were studied during macrophage differentiation and polarisation of monocytes isolated from healthy donors. The role of p16INK4A in MDMs from healthy donors was investigated by small interfering (si)RNA-mediated silencing or adenovirus-mediated overproduction of p16INK4A. Compared with MDMs and AMs, ATMs from obese patients expressed lower levels of p16
INK4A
. In vitro, IL-4-induced M2 polarisation resulted in lower p16INK4A protein levels after differentiation of monocytes from healthy donors in macrophages. Silencing of p16INK4A in MDMs mediated by siRNA increased the expression of M2 marker genes and enhanced the response to lipopolysaccharide (LPS), to give a phenotype resembling that of ATM. By contrast, adenovirus-mediated overproduction of p16INK4A in MDMs diminished M2 marker gene expression and the response to LPS. Western blot analysis revealed that p16INK4A overproduction inhibits LPS- and palmitate-induced Toll-like receptor 4 (TLR4)–nuclear factor of κ light polypeptide gene enhancer in B cells (NF-κB) signalling. These results show that p16INK4A inhibits the acquisition of the ATM phenotype. The age-related increase in p16INK4A level may thus influence normal ATM function and contribute to type 2 diabetes risk.
datePublished:2011-10-04T00:00:00Z
dateModified:2011-10-04T00:00:00Z
pageStart:3150
pageEnd:3156
sameAs:https://doi.org/10.1007/s00125-011-2324-0
keywords:
Adipose tissue macrophage
CDKN2A
Inflammation
Macrophage polarisation
Senescence
Type 2 diabetes
Internal Medicine
Metabolic Diseases
Human Physiology
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- What's the financial outcome of https://support.springernature.com/en/support/solutions/articles/6000255911-subscription-cancellations?
- Monthly income for https://www.springernature.com/
Analytics and Tracking {📊}
- Google Tag Manager
Libraries {📚}
- Clipboard.js
- Prism.js
CDN Services {📦}
- Crossref