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The role of focal adhesion kinase in transforming growth factor-β2 induced migration of human lens epithelial cells.

The migration of lens epithelial cells towards the posterior capsule is a key event in the development of posterior capsule opacification (PCO). Accumulating evidence has described crosstalk between growth factors and adhesive signaling pathways in wound healing and cell migration. The aim of the pr... Full description

Journal Title: International journal of molecular medicine December 2018, Vol.42(6), pp.3591-3601
Main Author: Liu, Jie
Other Authors: Xu, Dan , Li, Jingming , Gao, Ning , Liao, Chongbing , Jing, Ruihua , Wu, Bogang , Ma, Bo , Shao, Yongping , Pei, Cheng
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1791-244X ; DOI: 10.3892/ijmm.2018.3912
Link: http://search.proquest.com/docview/2116120950/?pq-origsite=primo
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recordid: proquest2116120950
title: The role of focal adhesion kinase in transforming growth factor-β2 induced migration of human lens epithelial cells.
format: Article
creator:
  • Liu, Jie
  • Xu, Dan
  • Li, Jingming
  • Gao, Ning
  • Liao, Chongbing
  • Jing, Ruihua
  • Wu, Bogang
  • Ma, Bo
  • Shao, Yongping
  • Pei, Cheng
subjects:
  • Animals–Enzymology
  • Capsule Opacification–Pathology
  • Cell Line–Drug Effects
  • Cell Movement–Cytology
  • Epithelial Cells–Drug Effects
  • Fibronectins–Enzymology
  • Focal Adhesion Protein-Tyrosine Kinases–Metabolism
  • Humans–Metabolism
  • Integrin Alpha5beta1–Metabolism
  • Lens, Crystalline–Cytology
  • Male–Pharmacology
  • Rabbits–Pharmacology
  • Signal Transduction–Pharmacology
  • Transforming Growth Factor Beta2–Pharmacology
  • Fibronectins
  • Integrin Alpha5beta1
  • Transforming Growth Factor Beta2
  • Focal Adhesion Protein-Tyrosine Kinases
ispartof: International journal of molecular medicine, December 2018, Vol.42(6), pp.3591-3601
description: The migration of lens epithelial cells towards the posterior capsule is a key event in the development of posterior capsule opacification (PCO). Accumulating evidence has described crosstalk between growth factors and adhesive signaling pathways in wound healing and cell migration. The aim of the present study was to elucidate an aberrant transforming growth factor (TGF)-[beta]2 signaling pathway that regulated the migration of lens epithelial cells in the pathological context of PCO. The expression of fibronectin, focal adhesion kinase (FAK) and phosphorylated (p)-FAK in HLE-B3 cells following TGF-[beta]2 treatment was determined by western blot analysis and the expression of integrin [alpha]5[beta]1 was detected by flow cytometry. Cell migration capacity was measured by wound healing and Transwell assays in the presence of 1,2,4,5-tetraaminobenzene tetrahydrochloride, a selective FAK inhibitor, fibronectin small interfering RNA interference, arginylglycylaspartic acid peptides or [alpha]5[beta]1-integrin neutralizing antibodies. The 1,2,4,5-tetraaminobenzene tetrahydrochloride was administered daily to 16 rabbits following cataract surgery. Fibronectin and TGF-[beta] expression were increased in the PCO group, demonstrated by immunofluorescence assays. PCO grading was conducted by slit-lamp biomicroscopy and evaluation of posterior capsule opacification software. It was observed that TGF-[beta]2 promoted HLE-B3 cell migration and upregulated fibronectin expression, which was followed by an increased phosphorylation of FAK. In addition, TGF-[beta]2 treatment and fibronectin surface coating significantly increased cell migration and FAK activation, which was inhibited by disrupting fibronectin-integrin [alpha]5[beta]1 interaction with the arginylglycylaspartic acid peptide, [alpha]5[beta]1-integrin neutralizing antibody or fibronectin depletion. Finally, suppression of FAK signaling by its inhibitor significantly decreased cell migration in vitro and attenuated PCO development in vivo. In summary, TGF-[beta]2 was indicated to promote the migration of lens epithelial cells through the TGF-[beta]2/fibronectin/integrin/FAK axis. Inhibition of FAK activity decreased TGF-[beta]2-mediated cell migration in vitro and improved the symptoms of PCO in a rabbit model.
language: eng
source:
identifier: E-ISSN: 1791-244X ; DOI: 10.3892/ijmm.2018.3912
fulltext: fulltext
issn:
  • 1791244X
  • 1791-244X
url: Link


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titleThe role of focal adhesion kinase in transforming growth factor-β2 induced migration of human lens epithelial cells.
creatorLiu, Jie ; Xu, Dan ; Li, Jingming ; Gao, Ning ; Liao, Chongbing ; Jing, Ruihua ; Wu, Bogang ; Ma, Bo ; Shao, Yongping ; Pei, Cheng
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identifierE-ISSN: 1791-244X ; DOI: 10.3892/ijmm.2018.3912
subjectAnimals–Enzymology ; Capsule Opacification–Pathology ; Cell Line–Drug Effects ; Cell Movement–Cytology ; Epithelial Cells–Drug Effects ; Fibronectins–Enzymology ; Focal Adhesion Protein-Tyrosine Kinases–Metabolism ; Humans–Metabolism ; Integrin Alpha5beta1–Metabolism ; Lens, Crystalline–Cytology ; Male–Pharmacology ; Rabbits–Pharmacology ; Signal Transduction–Pharmacology ; Transforming Growth Factor Beta2–Pharmacology ; Fibronectins ; Integrin Alpha5beta1 ; Transforming Growth Factor Beta2 ; Focal Adhesion Protein-Tyrosine Kinases
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descriptionThe migration of lens epithelial cells towards the posterior capsule is a key event in the development of posterior capsule opacification (PCO). Accumulating evidence has described crosstalk between growth factors and adhesive signaling pathways in wound healing and cell migration. The aim of the present study was to elucidate an aberrant transforming growth factor (TGF)-[beta]2 signaling pathway that regulated the migration of lens epithelial cells in the pathological context of PCO. The expression of fibronectin, focal adhesion kinase (FAK) and phosphorylated (p)-FAK in HLE-B3 cells following TGF-[beta]2 treatment was determined by western blot analysis and the expression of integrin [alpha]5[beta]1 was detected by flow cytometry. Cell migration capacity was measured by wound healing and Transwell assays in the presence of 1,2,4,5-tetraaminobenzene tetrahydrochloride, a selective FAK inhibitor, fibronectin small interfering RNA interference, arginylglycylaspartic acid peptides or [alpha]5[beta]1-integrin neutralizing antibodies. The 1,2,4,5-tetraaminobenzene tetrahydrochloride was administered daily to 16 rabbits following cataract surgery. Fibronectin and TGF-[beta] expression were increased in the PCO group, demonstrated by immunofluorescence assays. PCO grading was conducted by slit-lamp biomicroscopy and evaluation of posterior capsule opacification software. It was observed that TGF-[beta]2 promoted HLE-B3 cell migration and upregulated fibronectin expression, which was followed by an increased phosphorylation of FAK. In addition, TGF-[beta]2 treatment and fibronectin surface coating significantly increased cell migration and FAK activation, which was inhibited by disrupting fibronectin-integrin [alpha]5[beta]1 interaction with the arginylglycylaspartic acid peptide, [alpha]5[beta]1-integrin neutralizing antibody or fibronectin depletion. Finally, suppression of FAK signaling by its inhibitor significantly decreased cell migration in vitro and attenuated PCO development in vivo. In summary, TGF-[beta]2 was indicated to promote the migration of lens epithelial cells through the TGF-[beta]2/fibronectin/integrin/FAK axis. Inhibition of FAK activity decreased TGF-[beta]2-mediated cell migration in vitro and improved the symptoms of PCO in a rabbit model.
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