title: Interleukin-1 beta induces cardiac myocyte growth but inhibits cardiac fibroblast proliferation in culture.
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 anti-proliferative 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.
authors.affiliation: Cardiology Section, San Francisco Veterans Affairs Medical Center, California, USA.
authors.forename: J N
authors.initials: JN
authors.lastname: Palmer
authors.forename: W E
authors.initials: WE
authors.lastname: Hartogensis
authors.forename: M
authors.initials: M
authors.lastname: Patten
authors.forename: F D
authors.initials: FD
authors.lastname: Fortuin
authors.forename: C S
authors.initials: CS
authors.lastname: Long
mesh_terms: D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D019743:Chemokines, CXC; D002630:Chemotactic Factors / Q000378:metabolism; D004247:DNA / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D005347:Fibroblasts / Q000166:cytology; D015870:Gene Expression; D019833:Genistein; D006133:Growth Substances / Q000378:metabolism; D066298:In Vitro Techniques; D036341:Intercellular Signaling Peptides and Proteins; D007371:Interferon-gamma / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology*; D015850:Interleukin-6 / Q000494:pharmacology; D007529:Isoflavones / Q000494:pharmacology; D009124:Muscle Proteins / Q000096:biosynthesis; D009206:Myocardium / Q000166:cytology*; D009569:Nitric Oxide / Q000502:physiology; D011453:Prostaglandins / Q000502:physiology; D011493:Protein Kinase C / Q000502:physiology; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D011994:Recombinant Proteins; D015290:Second Messenger Systems
chemical_list: D019743:Chemokines, CXC; D002630:Chemotactic Factors; D006133:Growth Substances; D036341:Intercellular Signaling Peptides and Proteins; D007375:Interleukin-1; D015850:Interleukin-6; D007529:Isoflavones; D009124:Muscle Proteins; D011453:Prostaglandins; D012333:RNA, Messenger; D011994:Recombinant Proteins; D009569:Nitric Oxide; D007371:Interferon-gamma; D004247:DNA; D019833:Genistein; D011505:Protein-Tyrosine Kinases; D011493:Protein Kinase C