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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptNIH Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
PMC full text:
Int J Biochem Cell Biol. Author manuscript; available in PMC Aug 11, 2008.
Published in final edited form as:
Int J Biochem Cell Biol. 2006; 38(10): 1625–1631.
Published online Apr 3, 2006. doi:  10.1016/j.biocel.2006.03.010

Fig. 2

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Cellular interactions during corneal repair. (A) Upon corneal epithelial injury, IL-1α is released from the injured epithelium into the stroma. IL-1α induces some of the underlying stromal keratocytes to undergo cell death, while others are induced to proliferate, secrete MMPs, and transition from a quiescent to an activated phenotype. Due to the absence of a basement membrane, corneal epithelial cells also secrete TGFβ2 into the underlying stroma inducing a subpopulation of keratocytes to undergo transformation into myofibroblasts that secrete ECM. (B) The return of the basement membrane inhibits the release of TGFβ2 into the stroma and the myofibroblast phenotype is no longer observed. The activated keratocytes continue to secrete autocrine IL-1α and remodel the ECM. Abbreviations: MMPs, matrix metalloproteinase; TGFβ2, transforming growth factor beta; ECM, extracellular matrix; IL-1α, interleukin 1 alpha.

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