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J Biol Chem, Vol. 273, Issue 40, 25796-25803, October 2, 1998

Cardiac Fibroblasts Arrest at the G₁/S Restriction Point in Response to Interleukin (IL)-1
EVIDENCE FOR IL-1-INDUCED HYPOPHOSPHORYLATION OF THE RETINOBLASTOMA PROTEIN

From the Division of Cardiology and the Research Service, Veterans Affairs Medical Center, San Francisco, California 94121, and the Cardiovascular Research Institute and Department of Medicine, University of California, San Francisco, California 94143

Although responsible for only approximately one-third of the overall myocardial mass, the interstitial fibroblasts of the heart serve a fundamental role in establishing the functional integrity of myocardium and are the major source of myocardial extracellular matrix production. Their importance in clinical medicine is underscored by the observation that fibroblast numbers increase in response to several pathologic circumstances that are associated with an increase in extracellular matrix production, such as long standing hypertension and myocardial injury/infarction. Up to the present time, however, there has been little information available on either the kinetics of the cardiac fibroblast cell cycle, or the fundamental mechanisms that regulate its entry into and exit from the cell cycle. Previous work from our laboratory examining the effects of interleukin (IL)-1 on myocardial growth and gene expression in culture indicated that cardiac fibroblasts have a diminished capacity to synthesize DNA in response to mitogen in the presence of this cytokine. The mechanism of IL-1 action was not clear, however, and could have resulted from action at several different points in the cell cycle. The investigations described in this report indicate that IL-1 exerts its effect on the fibroblast cell cycle at multiple levels through altering the expression of cardiac fibroblast cyclins, cyclin-dependent kinases, and their inhibitors, which ultimately affect the phosphorylation of the retinoblastoma gene product.

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