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J. Biol. Chem., Vol. 279, Issue 4, 2832-2840, January 23, 2004

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Secreted Frizzled-related Protein 1 (SFRP1) Protects Fibroblasts from Ceramide-induced Apoptosis^*

Xiaozhe Han and Salomon Amar

From the Department of Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston University, Boston, Massachusetts 02118

Secreted frizzled-related proteins (SFRPs) are soluble proteins that have highly restricted tissue distribution. Although not fully understood, a role of SFRP1 in the regulation of apoptosis has been suggested. Our previous study disclosed a much greater level of SFRP1 expression in periodontal ligament fibroblasts (PDLFs), which have been suggested to maintain a reduced level of apoptosis compared with gingival fibroblasts. We have tested the role of SFRP1 in the regulation of fibroblast apoptosis both in vitro and in vivo. Our data showed that SFRP1 was significantly up-regulated in cultured human PDLFs during ceramide-induced apoptosis. In vivo study demonstrated an increased SFRP1 expression in mice periodontal ligament during force-induced apoptosis. While inhibition of endogenous SFRP1 increased the percentage of cell death in cultured human PDLFs, exogenous SFRP1 substantially reduced apoptosis in cultured human gingival fibroblasts, which do not maintain a high level of endogenous SFRP1 expression. The effect of SFRP1 on apoptosis was linked to the regulation of several apoptosis-related genes, including p53, caspase-3, caspase-9, and BCL-2-interacting killer (BIK). Furthermore our results indicated that the addition of exogenous SFRP1 could reduce the level of apoptosis in dermal fibroblasts in vivo, and this effect was also linked to the regulation of similar apoptosis-related genes as observed in in vitro studies. Collectively our results suggest that the constitutive up-regulation of SFRP1 could be an adaptive cell survival mechanism inherent to functionally specialized fibroblasts, and the addition of SFRP1 may contribute to the inhibition of apoptosis in fibroblast-related cells.

Received for publication, July 25, 2003 , and in revised form, October 14, 2003.

^* This work was supported in part by NIDCR, National Institutes of Health Grant DE 12482 (to S. A.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental data.

To whom correspondence should be addressed: Boston University, 700 Albany St., W-201E, Boston, MA 02118. Tel.: 617-638-4983; Fax: 617-638-8549; E-mail: samar{at}bu.edu.

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