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Shizuya Saika, Kumi Shiai, Yuka Okada, Masayasu Miyajima, Richard R Behringer, Osamu Yamanaka; Loss of Muc16 induces activates Stat3 signal and IL-6 expression in conjunctiva and secondarily affects corneal wound healing in mice.. Invest. Ophthalmol. Vis. Sci. 2014;55(13):3650.
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To investigate the inflammatory process in conjuncitva of a Muc16-null (KO) mouse and affects of the loss of Muc16 on corneal epithelium and keratocytes post-epithelial debridement.
KO mice (n = 40) and C57/BL6 (wild type, WT) mice (n = 40) were used. Expression of phospho-Stat3, AP-1 components, intrerleukin 6 (IL-6) and tumor necrosis factor alpha in cornea and conjunctiva was examined in WTand KO mice. Epithelial cell proliferation was studied by using BrdU labeling. Finally, wound healing of a round defect (diameter: 2.0 mm) in corneal epithelium was measured. Keratocyte phenotype and macrophage invasion in the stroma were evaluated after epithelium was recovered.
Lacking Muc16 activated Stat3 signal as well as upregulated expression of IL-6 mRNA in conjunctiva. Loss of Muc16 accelerated wound healing of corneal epithelium. The incidence of myofibroblast appearance and macrophage invasion were more marked in KO stroma as compared with WT stroma after epithelium repair.
Lacking Muc16 secondarily affects the homeostasis of corneal epithelium and stroma. The mechanism might include upregulation of inflammatory signaling cascade, i. e., Stat3 signal, and IL-6 expression in KO conjunctiva.
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