4.7 Article

MFAP5 is related to obesity-associated adipose tissue and extracellular matrix remodeling and inflammation

Journal

OBESITY
Volume 23, Issue 7, Pages 1371-1378

Publisher

WILEY
DOI: 10.1002/oby.21103

Keywords

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Funding

  1. Finnish Academy [117844, 118590]
  2. EVO-fund of the Kuopio University Hospital 5254 from Ministry of Health and Social Affairs
  3. TEKES [40058/07]
  4. COST [BM0602]
  5. Sigrid Juselius Foundation
  6. Diabetes Research Foundation
  7. Nordic Centre of Excellence on 'Systems biology in controlled dietary interventions and cohort studies, (SYSDIET) [070014]
  8. Deutsche Forschungsgemeinschaft [WA 1096/3-3]
  9. Novo Nordisk Fonden [NNF14OC0010187] Funding Source: researchfish

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ObjectiveLow-grade inflammation is involved in adipose tissue (AT) and extracellular matrix (ECM) remodeling and induces deposition of ECM proteins in AT. We have previously shown that MFAP5 (microfibrillar-associated protein 5) expression decreases in AT after weight loss. The aim of this study was to investigate MFAP5 localization in human AT and gene expression in adipocytes and the role of MFAP5 in adipocyte metabolism and inflammation. MethodsMFAP5 protein localization and gene expression were studied with immunohistochemistry and quantitative reverse transcriptase PCR (RT-qPCR) in human subcutaneous AT and cultured Simpson-Golabi-Behmel syndrome (SGBS) adipocytes, respectively. The effect of MFAP5 knock-down by siRNA on gene expression and insulin action was examined with RT-qPCR, western blot, and insulin-stimulated glucose uptake. The effect of different cytokines on MFAP5 gene and protein expression was investigated in cultured human SGBS preadipocytes. ResultsMFAP5 protein was highly expressed in AT, and gene expression decreased during adipocyte differentiation in SGBS cells. Treatment of preadipocytes with TNF and TGF1 increased MFAP5 gene and protein expression. Furthermore, MFAP5 knock-down decreased the expression of genes involved in inflammation. ConclusionsOur results demonstrate that factors involving low-grade inflammation modulate MFAP5 expression and that the modified expression of MFAP5 may further regulate AT inflammation.

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