Please use this identifier to cite or link to this item: https://doi.org/10.1074/jbc.M110.108175
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dc.titleAngiopoietin-like 4 interacts with matrix proteins to modulate wound healing
dc.contributor.authorGoh, Y.Y.
dc.contributor.authorPal, M.
dc.contributor.authorChong, H.C.
dc.contributor.authorZhu, P.
dc.contributor.authorTan, M.J.
dc.contributor.authorPunugu, L.
dc.contributor.authorTan, C.K.
dc.contributor.authorHuang, R.-L.
dc.contributor.authorSze, S.K.
dc.contributor.authorTang, M.B.Y.
dc.contributor.authorDing, J.L.
dc.contributor.authorKersten, S.
dc.contributor.authorTan, N.S.
dc.date.accessioned2014-10-27T08:21:54Z
dc.date.available2014-10-27T08:21:54Z
dc.date.issued2010-10-22
dc.identifier.citationGoh, Y.Y., Pal, M., Chong, H.C., Zhu, P., Tan, M.J., Punugu, L., Tan, C.K., Huang, R.-L., Sze, S.K., Tang, M.B.Y., Ding, J.L., Kersten, S., Tan, N.S. (2010-10-22). Angiopoietin-like 4 interacts with matrix proteins to modulate wound healing. Journal of Biological Chemistry 285 (43) : 32999-33009. ScholarBank@NUS Repository. https://doi.org/10.1074/jbc.M110.108175
dc.identifier.issn00219258
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/100090
dc.description.abstractA dynamic cell-matrix interaction is crucial for a rapid cellular response to changes in the environment. Appropriate cell behavior in response to the changing wound environment is required for efficient wound closure. However, the way in which wound keratinocytes modify the wound environment to coordinate with such cellular responses remains less studied.Wedemonstrated that angiopoietin-like 4 (ANGPTL4) produced by wound keratinocytes coordinates cell-matrix communication. ANGPTL4 interacts with vitronectin and fibronectin in the wound bed, delaying their proteolytic degradation by metalloproteinases. This interaction does not interfere with integrinmatrix protein recognition and directly affects cell-matrix communication by altering the availability of intact matrix proteins. These interactions stimulate integrin- focal adhesion kinase, 14-3-3, and PKC-mediated signaling pathways essential for effective wound healing. The deficiency of ANGPTL4 in mice delays wound re-epithelialization. Further analysis revealed that cell migration was impaired in the ANGPTL4-deficient keratinocytes. Altogether, the findings provide molecular insight into a novel control of wound healing via ANGPTL4-dependent regulation of cell-matrix communication. Given the known role of ANGPTL4 in glucose and lipid homeostasis, it is a prime therapeutic candidate for the treatment of diabetic wounds. It also underscores the importance of cell-matrix communication during angiogenesis and cancer metastasis. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1074/jbc.M110.108175
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1074/jbc.M110.108175
dc.description.sourcetitleJournal of Biological Chemistry
dc.description.volume285
dc.description.issue43
dc.description.page32999-33009
dc.description.codenJBCHA
dc.identifier.isiut000283048200037
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