Hypoxia-induced inflammatory cytokine secretion in human adipose tissue stromovascular cells

Aims Hypoxia has been implicated as a cause of adipose tissue inflammation in obesity, although the inflammatory response of human adipose tissue to hypoxia is not well understood. The goal of this study was to define in vitro inflammatory responses of human adipose tissue to hypoxia and identify mo...

Celý popis

Uloženo v:

Podrobná bibliografie
Vydáno v:	Diabetologia Ročník 54; číslo 6; s. 1480 - 1490
Hlavní autoři:	O’Rourke, R. W., White, A. E., Metcalf, M. D., Olivas, A. S., Mitra, P., Larison, W. G., Cheang, E. C., Varlamov, O., Corless, C. L., Roberts, C. T., Marks, D. L.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Berlin/Heidelberg Springer-Verlag 01.06.2011 Springer Springer Nature B.V
Témata:	Adipocytes Adult Biological and medical sciences Body fat Cells, Cultured Cytokines Cytokines - metabolism Diabetes Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Endoplasmic reticulum Enzymes Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Gastrointestinal surgery Human Physiology Humans Hypoxia Hypoxia - physiopathology Inflammation Internal Medicine Intra-Abdominal Fat - metabolism Intra-Abdominal Fat - pathology Killer Cells, Natural - pathology Kinases Lymphocytes Macrophages - pathology Male MAP Kinase Kinase 4 - metabolism Medical sciences Medicine Medicine & Public Health Metabolic Diseases Metabolic disorders Middle Aged Obesity Obesity - metabolism Obesity - pathology p38 Mitogen-Activated Protein Kinases - metabolism Phosphorylation Science Subcutaneous Fat - metabolism Subcutaneous Fat - pathology T-Lymphocytes - pathology Thinness - metabolism Thinness - pathology Oregon United States > US Obesity Adipose tissue p38 JNK T cell Hypoxia Inflammation Macrophage Endocrinopathy Human Oxygen Secretion Diabetes mellitus Nutrition disorder Cytokine Environmental factor T-Lymphocyte Nutritional status
ISSN:	0012-186X, 1432-0428, 1432-0428
On-line přístup:	Získat plný text
Tagy:	Přidat tag Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!

Popis
Shrnutí:	Aims Hypoxia has been implicated as a cause of adipose tissue inflammation in obesity, although the inflammatory response of human adipose tissue to hypoxia is not well understood. The goal of this study was to define in vitro inflammatory responses of human adipose tissue to hypoxia and identify molecular mechanisms of hypoxia-induced inflammation. Methods The inflammatory milieu and responses of visceral (VAT) and subcutaneous (SAT) adipose tissue explants and purified stromovascular cells (SVFs) from obese and lean humans were studied in an in vitro hypoxic culture system using quantitative real-time PCR, ELISA, western blotting, immunofluorescence microscopy, flow cytometry and immunohistochemistry. Results Human adipose tissue in obesity demonstrates an increased leucocyte infiltrate that is greater in VAT than SAT and involves macrophages, T cells and natural killer (NK) cells. Hypoxic culture regulates inflammatory cytokine secretion and transcription of metabolic stress response genes in human adipose tissue SVF. Adipocyte diameter is increased and adipose tissue capillary density is decreased in obese participants. Inhibition of c-Jun terminal kinase (JNK) or p38 significantly attenuates hypoxia-induced SVF inflammatory responses. Hypoxia induces phosphorylation of p38 in adipose tissue. Conclusions Human adipose tissue in obesity is characterised by a depot-specific inflammatory cell infiltrate that involves not only macrophages, but also T cells and NK cells. Hypoxia induces inflammatory cytokine secretion by human adipose tissue SVF, the primary source of which is adipose tissue macrophages. These data implicate p38 in the regulation of hypoxia-induced inflammation and suggest that alterations in adipocyte diameter and adipose tissue capillary density may be potential underlying causes of adipose tissue hypoxia.
Bibliografie:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 content type line 23
ISSN:	0012-186X 1432-0428 1432-0428
DOI:	10.1007/s00125-011-2103-y