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Insulin-like growth factor-1 induces migration and expression of laminin-5 in cultured human corneal epithelial cells

Authors
 Hyung Keun Lee  ;  Joon H. Lee  ;  Min Kim  ;  Yoshinobu Kariya  ;  Kaoru Miyazaki  ;  Eung Kweon Kim 
Citation
 Investigative Ophthalmology & Visual Science, Vol.47(3) : 873-882, 2006 
Journal Title
 Investigative Ophthalmology & Visual Science 
ISSN
 0146-0404 
Issue Date
2006
MeSH
Blotting, Western ; Cell Adhesion Molecules/biosynthesis* ; Cell Movement/drug effects* ; Cells, Cultured ; Chromones/pharmacology ; Epithelium, Corneal/cytology* ; Epithelium, Corneal/metabolism* ; Flavonoids/pharmacology ; Fluorescent Antibody Technique, Indirect ; Humans ; Insulin-Like Growth Factor I/pharmacology* ; Integrin beta1/biosynthesis ; MAP Kinase Signaling System/drug effects ; Morpholines/pharmacology ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Receptor, IGF Type 1/antagonists & inhibitors ; Up-Regulation
Abstract
PURPOSE: The effects of insulin-like growth factor (IGF)-1 on laminin (Ln)-5 and the associated integrins during in vitro HCEC migration were examined. Also investigated were the effects of IGF-1 on the migration of human corneal epithelial cells (HCECs). METHODS: HCEC migration was examined by wound-healing and chemoattraction assays. For migration inhibition assays, HCECs were pretreated with inhibitors of the IGF-1 receptor (alphaIR3), the PI3-K/AKT pathway (LY294002), and the MEK-ERK pathway (PD98059). The expression levels of Ln-5 and fibronectin (Fn) were determined by Western blot analysis, and the expression levels of the beta1 and alpha3 integrins were determined by confocal microscopy and Western blot analysis. The migration inhibition with anti-integrin alpha3 and beta1 antibodies was also determined. RESULTS: HCEC migration was significantly increased in the presence of IGF-1 and Ln-5. IGF-1 enhanced the production of Ln-5 in both a dose- and time-dependent manner, and this upregulation was blocked by pretreatment with alphaIR3 or LY294002. IGF-1 treatment upregulated expression of beta1 integrin, but not alpha3 integrin. The HCEC migration facilitated by IGF-1 was inhibited with the anti-integrin antibody for beta1. However, there was no cross-talk between Ln-5 and integrin beta1 production. CONCLUSIONS: The results reveal that IGF-1 induces HCEC migration through the independent production of Ln-5 and beta1 integrin, which are directed at least in part by activation of the PI3-K/AKT pathway, but are not affected by the MEK-ERK pathway.
Files in This Item:
T200600016.pdf Download
DOI
10.1167/iovs.05-0826
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Min(김민) ORCID logo https://orcid.org/0000-0003-1873-6959
Kim, Eung Kweon(김응권) ORCID logo https://orcid.org/0000-0002-1453-8042
Lee, Joon Haeng(이준행)
Lee, Hyung Keun(이형근) ORCID logo https://orcid.org/0000-0002-1123-2136
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/108758
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