Volume 271, Number 37, Issue of September 13, 1996 pp. 22583-22590
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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Integrin Regulation by Endogenous Expression of 18-kDa Fibroblast Growth Factor-2

(Received for publication, February 15, 1996, and in revised form, May 30, 1996)

Sharon Klein , Andreas Bikfalvi ^¶ , Thomas M. Birkenmeier , Filippo G. Giancotti ^'' and Daniel B. Rifkin

From the Departments of  Cell Biology and ^'' Pathology, the  Raymond and Beverly Sackler Foundation Laboratory, and the Kaplan Cancer Center, New York University Medical Center, New York, New York 10016, the ^¶ Laboratory of Growth Factors and Cell Differentiation, University of Bordeaux I, Avenue des Facultés, 33405 Talence, France, and the  Department of Internal Medicine, Washington School of Medicine, St. Louis, Missouri 63110

The three high molecular weight (HMW) forms of fibroblast growth factor-2 (FGF-2) have a distinct intracellular localization and differentially affect cell mobility and growth compared with the fourth 18-kDa form. To characterize further the effects of the 18-kDa and HMW forms of FGF-2, we have examined their ability to modulate integrin expression. Transfected NIH 3T3 cells expressing only 18-kDa FGF-2 exhibited increased cell surface levels of 51, whereas cells expressing only HMW FGF-2 exhibited cell surface 51 levels similar to parental cells. When cells synthesizing 18-kDa FGF-2 were transfected with a cDNA encoding a dominant negative FGF receptor, 51 cell surface levels decreased. Immunoprecipitation of biosynthetically labeled cells indicated that expression of 18-kDa FGF-2 increased the biosynthesis and rate of maturation of 5. Northern blot analysis showed that 18-kDa FGF-2 increases the level of the 5 subunit mRNA but does not affect 1 subunit transcript levels. Experiments utilizing luciferase reporter gene activity revealed increased 5 promoter activity in cells expressing 18-kDa FGF-2 indicating that the enhanced 5 transcript level is due to modulation of the transcription rate. Therefore, interaction of 18-kDa FGF-2 with FGF receptors results in changes in 51 biosynthesis and processing. In contrast, endogenous expression of HMW FGF-2 does not mediate this effect.

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