A Peptide Derived from Tenascin-C Induces 1 Integrin Activation through Syndecan-4.

A Peptide Derived from Tenascin-C Induces 1 Integrin Activation through Syndecan-4. Research Abstract Details 

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A Peptide Derived from Tenascin-C Induces 1 Integrin Activation through Syndecan-4. Abstract Text:

Yohei Saito,Hisae Imazeki,Shogo Miura,Tomohisa Yoshimura,Hiroaki Okutsu,Yosei Harada,Toshiyuki Ohwaki,Osamu Nagao,Sadahiro Kamiya,Ryo Hayashi,Hiroaki Kodama,Hiroshi Handa,Toshimichi Yoshida,Fumio Fukai,Yohei Saito,Hisae Imazeki,Shogo Miura,Tomohisa Yoshimura,Hiroaki Okutsu,Yosei Harada,Toshiyuki Ohwaki,Osamu Nagao,Sadahiro Kamiya,Ryo Hayashi,Hiroaki Kodama,Hiroshi Handa,Toshimichi Yoshida,Fumio Fukai,Yohei Saito,Hisae Imazeki,Shogo Miura,Tomohisa Yoshimura,Hiroaki Okutsu,Yosei Harada,Toshiyuki Ohwaki,Osamu Nagao,Sadahiro Kamiya,Ryo Hayashi,Hiroaki Kodama,Hiroshi Handa,Toshimichi Yoshida,Fumio Fukai,

Tenascin-C (TN-C) is unique for its cell adhesion modulatory function. We have shown that TNIIIA2, a synthetic 22-mer peptide derived from TN-C, stimulated beta1 integrin-mediated cell adhesion of nonadherent and adherent cell types, by inducing activation of beta1 integrin. The active site of TNIIIA2 appeared cryptic in the TN-C molecule but was exposed by MMP-2 processing of TN-C. The following results suggest that cell surface heparan sulfate (HS) proteoglycan (HSPG), including syndecan-4, participated in TNIIIA2-induced beta1 integrin activation: 1) TNIIIA2 bound to cell surface HSPG via its HS chains, as examined by photoaffinity labeling; 2) heparitinase I treatment of cells abrogated beta1 integrin activation induced by TNIIIA2; 3) syndecan-4 was isolated by affinity chromatography using TNIIIA2-immobilized beads; 4) small interfering RNA-based down-regulation of syndecan-4 expression reduced TNIIIA2-induced beta1 integrin activation, and consequent cell adhesion to fibronectin; 5) overexpression of syndecan-4 core protein enhanced TNIIIA2-induced activation of beta1 integrin. However, treatments that targeted the cytoplasmic region of syndecan-4, including ectopic expression of its mutant truncated with the cytoplasmic domains and treatment with protein kinase Calpha inhibitor Gö6976, did not influence the TNIIIA2 activity. These results suggest that a TNIIIA2-related matricryptic site of the TN-C molecule, exposed by MMP-2 processing, may have bound to syndecan-4 via its HS chains and then induced conformational change in beta1 integrin necessary for its functional activation. A lateral interaction of beta1 integrin with the extracellular region of the syndecan-4 molecule may be involved in this conformation change.

A Peptide Derived from Tenascin-C Induces 1 Integrin Activation through Syndecan-4. Publishing Authors By Initials

Y Saito,H Imazeki,S Miura,T Yoshimura,H Okutsu,Y Harada,T Ohwaki,O Nagao,S Kamiya,R Hayashi,H Kodama,H Handa,T Yoshida,F Fukai,Y Saito,H Imazeki,S Miura,T Yoshimura,H Okutsu,Y Harada,T Ohwaki,O Nagao,S Kamiya,R Hayashi,H Kodama,H Handa,T Yoshida,F Fukai,Y Saito,H Imazeki,S Miura,T Yoshimura,H Okutsu,Y Harada,T Ohwaki,O Nagao,S Kamiya,R Hayashi,H Kodama,H Handa,T Yoshida,F Fukai,

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A Peptide Derived from Tenascin-C Induces 1 Integrin Activation through Syndecan-4. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: The Journal of biological chemistry

VOLUME: 282

Page Numbers: 34929-37

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 26

MONTH: 09

YEAR: 2007

A Peptide Derived from Tenascin-C Induces 1 Integrin Activation through Syndecan-4. Information

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LANGUAGE: eng

NlmUniqueID: 2985121

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AFFILIATION: Department of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.

Country: United States

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MEDLINETA: J Biol Chem

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