Thrombospondin-4 expression is rapidly upregulated by cardiac overload

Biochem Biophys Res Commun. 2008 Aug 22;373(2):186-91. doi: 10.1016/j.bbrc.2008.05.164. Epub 2008 Jun 9.


The precise mechanisms regulating gene expression of thrombospondins (TSPs) in the heart remain incompletely understood. Here we characterized cardiac TSP-4 expression in response to pressure overload and myocardial infarction in vivo. Arginine(8)-vasopressin (AVP) infusion increased left ventricular (LV) TSP-4 mRNA levels within 30 min. Also angiotensin II infusion rapidly activated LV TSP-4 expression, TSP-4 mRNA levels being highest at 6h and protein at 72 h and 2 weeks. During remodeling process following myocardial infarction, LV TSP-4 mRNA levels increased at day one, as studied by quantitative RT-PCR. TSP-4 immunostaining was localized to endothelial cells in hypertrophied hearts of spontaneously hypertensive rats. AVP-infusion increased LV TSP-1 mRNA levels similarly to TSP-4 within 30 min showing that rapid induction of gene expression, well before the development of cardiac hypertrophy, is typical for the thrombospondin family. These results further suggest that TSP-4 may be an endothelial specific marker of cardiac overload.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging
  • Animals
  • Biomarkers
  • Heart*
  • Male
  • Myocardial Infarction / genetics*
  • Pressure
  • Rats
  • Rats, Inbred Strains
  • Thrombospondin 1 / genetics
  • Thrombospondin 1 / metabolism
  • Thrombospondins / genetics*
  • Thrombospondins / metabolism
  • Transcriptional Activation*
  • Up-Regulation
  • Ventricular Remodeling / genetics*


  • Biomarkers
  • Thrombospondin 1
  • Thrombospondins
  • thrombospondin 4