Abstract
Betaig-h3 (βig-h3) is a secretory protein composed of fasciclin I-like repeats containing sequences that allows binding of integrins and glycosaminoglycans in vivo. Expression of βig-h3 is responsive to TGF-β and the protein is found to be associated with extracellular matrix (ECM) molecules, implicating βig-h3 as an ECM adhesive protein of developmental processes. We previously observed predominant expression of βig-h3 expression in the basement membrane of proximal tubules of kidney. In this study, the physiological relevance of such localized expression of βig-h3 was examined in the renal proximal tubular epithelial cells (RPTEC). RPTEC constitutively expressed βig-h3 and the expression was dramatically induced by exogenous TGF-β1 treatment. βig-h3 and its second and fourth FAS1 domain were able to mediate RPTEC adhesion, spreading and migration. Two known α3β1 integrin-interaction motifs including aspartatic acid and isoleucine residues, NKDIL and EPDIM in βig-h3 were responsible to mediate RPTEC adhesion, spreading, and migration. By using specific antibodies against integrins, we confirmed that α3β1 integrin mediates the adhesion and migration of RPTECs on βig-h3. In addition, it also enhanced proliferation of RPTECs through NKDIL and EPDIM. These results indicate that βig-h3 mediates adhesion, spreading, migration and proliferation of RPTECs through the interaction with α3β1 integrin and is intimately involved in the maintenance and the regeneration of renal proximal tubular epithelium.
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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Park, SW., Bae, JS., Kim, KS. et al. Beta ig-h3 promotes renal proximal tubular epithelial cell adhesion, migration and proliferation through the interaction with α3β1 integrin. Exp Mol Med 36, 211–219 (2004). https://doi.org/10.1038/emm.2004.29
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DOI: https://doi.org/10.1038/emm.2004.29
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