HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 280, Issue 22, 21629-21637, June 3, 2005

This Article Full Text Full Text (PDF) All Versions of this Article: 280/22/21629    most recent M412293200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Oh, J.-E. Articles by Min, B.-M. Search for Related Content PubMed PubMed Citation Articles by Oh, J.-E. Articles by Min, B.-M. Social Bookmarking                      What's this?

ig-h3 Induces Keratinocyte Differentiation via Modulation of Involucrin and Transglutaminase Expression through the Integrin 31 and the Phosphatidylinositol 3-Kinase/Akt Signaling Pathway^*

Ju-Eun Oh, Joong-Ki Kook, and Byung-Moo Min¶

From the Department of Oral Biochemistry and Craniomaxillofacial Reconstructive Sciences, Dental Research Institute, and BK21 HLS, Seoul National University College of Dentistry, Seoul 110-749, Korea and the Department of Oral Biochemistry, Chosun University College of Dentistry, Gwangju 501-759, Korea

ig-h3 is an extracellular matrix protein whose expression is highly induced by transforming growth factor (TGF)-1. Whereas ig-h3 is known to mediate keratinocyte adhesion and migration, its effects on keratinocyte differentiation remain unclear. In the present study, it was demonstrated that expression of both ig-h3 and TGF-1 was enhanced during keratinocyte differentiation and that expression of the former was strongly induced by that of the latter. This study also asked whether changes in -h3 expression would affect keratinocyte differentiation. Indeed, down-regulation of ig-h3 by transfection with antisense ig-h3 cDNA constructs effectively inhibited keratinocyte differentiation by decreasing the promoter activities and thus expression of involucrin and transglutaminase. The result was a 2-fold increase in mitotic capacity of the cells. Conversely, overexpression of ig-h3, either by transfection with ig-h3 expression plasmids or by exposure to recombinant ig-h3, enhanced keratinocyte differentiation by inhibiting cell proliferation and concomitantly increasing involucrin and transglutaminase expression. Recombinant ig-h3 also promoted keratinocyte adhesion through interaction with integrin 31. Changes in ig-h3 expression did not affect intracellular calcium levels. Subsequent analysis revealed not only induction of Akt phosphorylation by recombinant ig-h3 but also blockage of Akt phosphorylation by LY294002, an inhibitor of phosphatidylinositol 3-kinase. Taken together, these findings indicate that enhanced ig-h3, induced by enhanced TGF- during keratinocyte differentiation, provoked cell differentiation by enhancing involucrin and transglutaminase expression through the integrin 31 and phosphatidylinositol 3-kinase/Akt signaling pathway. Lastly, it was observed that ig-h3-mediated keratinocyte differentiation was caused by promotion of cell adhesion and not by calcium regulation.

Received for publication, October 29, 2004 , and in revised form, March 7, 2005.

^* This work was supported by Korea Health 21 R&D Project Grant 02-PJ1-PG3-20507-0038, Ministry of Health & Welfare, Republic of Korea (to B.-M. M.). 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.

^¶ To whom correspondence should be addressed: Dept. of Oral Biochemistry and Craniomaxillofacial Reconstructive Sciences, Seoul National University College of Dentistry, 28 Yeonkun-Dong, Chongno-Ku, Seoul 110-749, Korea. Tel.: 82-2-740-8661; Fax: 82-2-740-8665; E-mail: bmmin{at}snu.ac.kr.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				S.-H. Park, S.-Y. Choi, M.-H. Kim, E.-J. Oh, H. M. Ryu, C.-D. Kim, I.-S. Kim, and Y.-L. Kim The TGF- -induced gene product, ig-h3: its biological implications in peritoneal dialysis Nephrol. Dial. Transplant., January 1, 2008; 23(1): 126 - 135. [Abstract] [Full Text] [PDF]

				J. Becker, B. Erdlenbruch, I. Noskova, A. Schramm, M. Aumailley, D. F. Schorderet, and L. Schweigerer Keratoepithelin suppresses the progression of experimental human neuroblastomas. Cancer Res., May 15, 2006; 66(10): 5314 - 5321. [Abstract] [Full Text] [PDF]

				B. Reinboth, J. Thomas, E. Hanssen, and M. A. Gibson betaig-h3 Interacts Directly with Biglycan and Decorin, Promotes Collagen VI Aggregation, and Participates in Ternary Complexing with These Macromolecules J. Biol. Chem., March 24, 2006; 281(12): 7816 - 7824. [Abstract] [Full Text] [PDF]