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Volume 272, Number 23, Issue of June 6, 1997 pp. 14617-14623
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Transforming Growth Factor-beta 1 Inhibits Type I Inositol 1,4,5-Trisphosphate Receptor Expression and Enhances Its Phosphorylation in Mesangial Cells

(Received for publication, January 10, 1997, and in revised form, March 18, 1997)

Kumar Sharma Dagger , Lewei Wang Dagger , Yanqing Zhu Dagger , Shaila Bokkala and Suresh K. Joseph

From the Dagger  Department of Medicine, Nephrology Division and the  Department of Anatomy, Pathology, and Cell Biology, Thomas Jefferson University School of Medicine, Philadelphia, Pennsylvania 19107

A potentially important cross-talk characteristic of transforming growth factor-beta (TGF-beta ) is to inhibit platelet-derived growth factor-induced intracellular calcium rise (Baffy, G., Sharma, K., Shi, W., Ziyadeh, F. N., and Williamson, J. R. (1995) Biochem. Biophys. Res. Commun. 210, 378-383) in murine mesangial cells. The present study examined the possible basis for this effect by evaluating the regulation of the type I inositol 1,4,5-trisphosphate receptor (IP3R) by TGF-beta . TGF-beta 1 down-regulates IP3R protein expression by >90% with maximal and half-maximal effects after 8 and 2 h, respectively. TGF-beta 1 also decreased IP3R mRNA expression by 59% after 1 h. Phosphorylation of the IP3R was also demonstrated as early as 15 min after TGF-beta 1 exposure. Back phosphorylation assays of IP3R from TGF-beta 1-treated mesangial cells with protein kinase A (PKA), indicated that TGF-beta 1-induced phosphorylation of the IP3R occurs at similar sites as for PKA. In vitro kinase assays using the known IP3R peptide substrates for PKA, RPSGRRESLTSFGNP and ARRDSVLAAS, demonstrated that TGF-beta 1 induces phosphorylation of both peptides (158 and 123% of control values, respectively). TGF-beta 1-induced phosphorylation was prevented by the addition of the PKA inhibitor peptide in the in vitro kinase assay. It is proposed that TGF-beta -mediated effects on the IP3R may be an important characteristic of its ability to modulate the response of cells to factors that employ IP3R-mediated calcium release.


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