Loss of osteopontin perturbs the epithelial-mesenchymal transition in an injured mouse lens epithelium.

Loss of osteopontin perturbs the epithelial-mesenchymal transition in an injured mouse lens epithelium. Research Abstract Details 

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Loss of osteopontin perturbs the epithelial-mesenchymal transition in an injured mouse lens epithelium. Abstract Text:

Shizuya Saika,Kumi Shirai,Osamu Yamanaka,Ken-Ichi Miyazaki,Yuka Okada,Ai Kitano,Kathleen C Flanders,Shigeyuki Kon,Toshimitsu Uede,Winston Whei-Yang Kao,Susan R Rittling,David T Denhardt,Yoshitaka Ohnishi,

We previously reported that osteopontin (OPN), a matrix structural glycophosphoprotein, is upregulated in the injured mouse lens prior to the epithelial-mesenchymal transition (EMT). Here, we investigated the role of this protein in EMT of the lens epithelium during wound healing. The crystalline lens was injured by needle puncture in OPN-null (KO, n=40) and wild-type (WT, n=40) mice. The animals were killed at day 1, 2, 5, and 10 postinjury. Immunohistochemistry was employed to detect alpha-smooth muscle action (alphaSMA), a marker of EMT, collagen type I, transforming growth factor beta1 (TGFbeta1), TGFbeta2, and phospho-Smad2/3. Cell proliferation was assayed by examining uptake of bromodeoxyuridine (BrdU). The results showed that injury-induced EMT of mouse lens epithelium, as evaluated by histology, expression pattern of alphaSMA and collagen I, was altered in the absence of OPN with reduced phospho-Smad2/3 signaling. Upregulation of TGFbeta1 and TGFbeta2 in the epithelium was also inhibited. Cell proliferation was more active in KO mice as compared with WT mice at day 1 and 2, but not at day 5 and 10. An in vitro experiment shows OPN facilitates cell adhesion of lens epithelial cell line. OPN is required for activation of Smad2/3 signal in an injured lens epithelium and lens cell EMT.

Loss of osteopontin perturbs the epithelial-mesenchymal transition in an injured mouse lens epithelium. Publishing Authors By Initials

S Saika,K Shirai,O Yamanaka,K Miyazaki,Y Okada,A Kitano,KC Flanders,S Kon,T Uede,WW Kao,SR Rittling,DT Denhardt,Y Ohnishi,

For similar biological phenomena, cell phenomena, and immunity: biological phenomena: regeneration: wound healing research abstracts see: biological phenomena, cell phenomena, and immunity: biological phenomena: regeneration: wound healing research

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Loss of osteopontin perturbs the epithelial-mesenchymal transition in an injured mouse lens epithelium. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Laboratory investigation; a journal of technical m

VOLUME: 87

Page Numbers: 130-8

Journal Abbreviation: Lab. Invest.

ISSN: 0023-6837

DAY: 8

MONTH: 01

YEAR: 2007

Loss of osteopontin perturbs the epithelial-mesenchymal transition in an injured mouse lens epithelium. Information

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LANGUAGE: eng

NlmUniqueID: 376617

Loss of osteopontin perturbs the epithelial-mesenchymal transition in an injured mouse lens epithelium. Keywords Mesh Terms:

KEYWORDS: Wound Healing

MESH TERMS: physiology

Chemical & Substance for Abstract: Loss of osteopontin perturbs the epithelial-mesenchymal transition in an injured mouse lens epithelium. Information

Substance Name: Bromodeoxyuridine

Registry Number: 59-14-3

Grant and Affiliation Information for Loss of osteopontin perturbs the epithelial-mesenchymal transition in an injured mouse lens epithelium.

AFFILIATION: Department of Ophthalmology, Wakayama Medical University, Wakayama, Japan. shizuya@wakayama-med.ac.jp

Country: United States

AGENCY: United States NEI

GRANT: EY13755

ACRONYM: EY

MEDLINETA: Lab Invest

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