Characterization of the long pentraxin PTX3 as a TNFalpha-induced secreted protein of adipose cells

J Lipid Res. 2003 May;44(5):994-1000. doi: 10.1194/jlr.M200382-JLR200. Epub 2003 Mar 1.

Abstract

Exposure of preadipocytes to long-chain fatty acids induces the expression of several markers of adipocyte differentiation. In an attempt to identify novel genes and proteins that are regulated by fatty acids in preadipocytes, we performed a substractive hybridization screening and identified PTX3, a protein of the pentraxin family. PTX3 mRNA expression is transient during adipocyte differentiation of clonal cell lines and is absent in fully differentiated cells. Stable overexpression of PTX3 in preadipocytes has no effect on adipocyte differentiation. In line with this, PTX3 mRNA is expressed in the stromal-vascular fraction of adipose tissue, but not in the adipocyte fraction; however, in 3T3-F442A adipocytes, the PTX3 gene can be reinduced by tumor necrosis factor alpha (TNFalpha) in a dose-dependent manner. This effect is accompanied by PTX3 protein secretion from both 3T3-F442A adipocytes and explants of mouse adipose tissue. PTX3 mRNA levels are found to be higher in adipose tissue of genetically obese mice versus control mice, consistent with their increased TNFalpha levels. In conclusion, PTX3 appears as a TNFalpha-induced protein that provides a new link between chronic low-level inflammatory state and obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Adipocytes / cytology
  • Adipocytes / drug effects
  • Adipocytes / metabolism*
  • Adipose Tissue / cytology
  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism*
  • Animals
  • C-Reactive Protein / genetics*
  • C-Reactive Protein / metabolism
  • Cell Differentiation / drug effects
  • Cell Differentiation / physiology
  • Diabetes Mellitus / genetics
  • Gene Expression Regulation, Developmental / drug effects
  • Mice
  • Mice, Obese
  • Obesity
  • RNA, Messenger / drug effects
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Serum Amyloid P-Component / genetics*
  • Serum Amyloid P-Component / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • RNA, Messenger
  • Serum Amyloid P-Component
  • Tumor Necrosis Factor-alpha
  • PTX3 protein
  • C-Reactive Protein