Interleukin-1β induces cardiac myocyte growth but inhibits cardiac fibroblast proliferation in culture

James N. Palmer, Wendy E. Hartogensis, Monica Patten, F. David Fortuin, Carlin S. Long

Research output: Contribution to journalArticle

156 Scopus citations

Abstract

Interleukin-1 (IL-1), initially called 'endogenous pyrogen,' is primarily known as a mediator of inflammation. However, it also plays many other diverse physiologic roles including the stimulation and inhibition of both primary cells in culture and the interstitial and parenchymal cells of a number of organs including the heart. In the heart, IL-1 expression has traditionally been reported in situations where there is immunologic myocardial injury such as occurs during transplant rejection and congestive heart failure. For this reason, all of the effects of IL-1 have been presumed to be deleterious. Using a cell culture model which allows both the muscle cells (myocytes) and nonmuscle cells (fibroblasts) to be evaluated separately, we have found that IL-1 induces both cardiac myocyte hypertrophy and reinitiates myocyte DNA synthesis. In stark contrast, IL-1 exerts a potent antiproliferative effect on cardiac fibroblasts. To our knowledge this is the first report concerning the differential effects of IL-1 on myocardial cell growth in culture and, given the inducible expression of IL-1 by myocardial cells during stress, underscores the importance of investigating the complex nature of the intracardiac cell-cell interactions that occur in the heart.

Original languageEnglish (US)
Pages (from-to)2555-2564
Number of pages10
JournalJournal of Clinical Investigation
Volume95
Issue number6
DOIs
StatePublished - Jun 1995

Keywords

  • cardiac fibroblast
  • cardiac myocyte
  • hypertrophy
  • interleukin-1

ASJC Scopus subject areas

  • Medicine(all)

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