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Increased importin 13 activity is associated with the pathogenesis of pterygium.

PURPOSEWe previously reported that importin 13 (IPO13), a member of the importin-β family of nuclear import proteins, regulates nuclear import of the glucocorticoid receptor in airway epithelial cells, IPO13 serves as a potential marker for corneal epithelial progenitor cells, and IPO13 is associate... Full description

Journal Title: Molecular vision 2013, Vol.19, pp.604-613
Main Author: Xu, Ke
Other Authors: Tao, Tao , Jie, Jing , Lu, Xiaodong , Li, Xuezhi , Mehmood, Muhammad Aamer , He, Hui , Liu, Zhen , Xiao, Xinye , Yang, Jie , Ma, Jian-Xing , Li, Wei , Zhou, Yueping , Liu, Zuguo
Format: Electronic Article Electronic Article
Language: English
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ID: E-ISSN: 1090-0535 ; DOI: 1090-0535
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title: Increased importin 13 activity is associated with the pathogenesis of pterygium.
format: Article
creator:
  • Xu, Ke
  • Tao, Tao
  • Jie, Jing
  • Lu, Xiaodong
  • Li, Xuezhi
  • Mehmood, Muhammad Aamer
  • He, Hui
  • Liu, Zhen
  • Xiao, Xinye
  • Yang, Jie
  • Ma, Jian-Xing
  • Li, Wei
  • Zhou, Yueping
  • Liu, Zuguo
subjects:
  • Adult–Metabolism
  • Aged–Metabolism
  • Cell Nucleus–Pathology
  • Cell Proliferation–Metabolism
  • Cells, Cultured–Pathology
  • Epithelial Cells–Genetics
  • Epithelium–Metabolism
  • Female–Genetics
  • Gene Expression Regulation–Metabolism
  • Gene Silencing–Etiology
  • Humans–Genetics
  • Karyopherins–Metabolism
  • Keratin-17–Pathology
  • Male–Metabolism
  • Middle Aged–Metabolism
  • Protein Transport–Metabolism
  • Pterygium–Metabolism
  • Transcription Factor AP-1–Metabolism
  • Karyopherins
  • Keratin-17
  • Transcription Factor AP-1
  • Importin 13, Human
ispartof: Molecular vision, 2013, Vol.19, pp.604-613
description: PURPOSEWe previously reported that importin 13 (IPO13), a member of the importin-β family of nuclear import proteins, regulates nuclear import of the glucocorticoid receptor in airway epithelial cells, IPO13 serves as a potential marker for corneal epithelial progenitor cells, and IPO13 is associated with corneal cell proliferation. Here we investigated the role of IPO13 in the pathogenesis of pterygium and the underlying mechanism including interaction with other cell proliferation-related factors: keratin 17 (K17), a lesional protein and a member of the type I keratins, and c-Jun, a protein of the activator protein-1 complex. METHODSTissue samples were collected from primary pterygia, recurrent pterygia, and normal conjunctiva to perform the following experiments: immunohistochemical measurement of IPO13 and K17. Pterygium epithelial cells (PECs) were cultured in keratinocyte serum-free defined medium to examine the expression of IPO13 and K17. Lentivirus-mediated silencing and overexpression IPO13 testing was conducted, and K17 alternation was evaluated with western blot and immunostaining. In addition, the translocation of c-Jun (a K17 regulator) was further examined after IPO13 was silenced. RESULTSIPO13 activity was significantly increased in the basal layer of the epithelium of the pterygium. In cultured PECs, overexpression or knockdown of the IPO13 gene increased or decreased PEC proliferation, respectively. IPO13 was colocalized with K17 in the epithelium of the pterygium, and overexpression or knockdown of the IPO13 gene induced upregulation or downregulation of K17 expression in PECs, respectively. In addition, silencing of the IPO13 gene blocked nuclear translocation of c-Jun. CONCLUSIONSWe provided novel evidence that IPO13 may contribute to the pathogenesis of pterygium via modulation of K17 and c-Jun.
language: eng
source: © ProQuest LLC All rights reserved
identifier: E-ISSN: 1090-0535 ; DOI: 1090-0535
fulltext: fulltext
issn:
  • 10900535
  • 1090-0535
url: Link


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titleIncreased importin 13 activity is associated with the pathogenesis of pterygium.
creatorXu, Ke ; Tao, Tao ; Jie, Jing ; Lu, Xiaodong ; Li, Xuezhi ; Mehmood, Muhammad Aamer ; He, Hui ; Liu, Zhen ; Xiao, Xinye ; Yang, Jie ; Ma, Jian-Xing ; Li, Wei ; Zhou, Yueping ; Liu, Zuguo
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ispartofMolecular vision, 2013, Vol.19, pp.604-613
identifierE-ISSN: 1090-0535 ; DOI: 1090-0535
subjectAdult–Metabolism ; Aged–Metabolism ; Cell Nucleus–Pathology ; Cell Proliferation–Metabolism ; Cells, Cultured–Pathology ; Epithelial Cells–Genetics ; Epithelium–Metabolism ; Female–Genetics ; Gene Expression Regulation–Metabolism ; Gene Silencing–Etiology ; Humans–Genetics ; Karyopherins–Metabolism ; Keratin-17–Pathology ; Male–Metabolism ; Middle Aged–Metabolism ; Protein Transport–Metabolism ; Pterygium–Metabolism ; Transcription Factor AP-1–Metabolism ; Karyopherins ; Keratin-17 ; Transcription Factor AP-1 ; Importin 13, Human
descriptionPURPOSEWe previously reported that importin 13 (IPO13), a member of the importin-β family of nuclear import proteins, regulates nuclear import of the glucocorticoid receptor in airway epithelial cells, IPO13 serves as a potential marker for corneal epithelial progenitor cells, and IPO13 is associated with corneal cell proliferation. Here we investigated the role of IPO13 in the pathogenesis of pterygium and the underlying mechanism including interaction with other cell proliferation-related factors: keratin 17 (K17), a lesional protein and a member of the type I keratins, and c-Jun, a protein of the activator protein-1 complex. METHODSTissue samples were collected from primary pterygia, recurrent pterygia, and normal conjunctiva to perform the following experiments: immunohistochemical measurement of IPO13 and K17. Pterygium epithelial cells (PECs) were cultured in keratinocyte serum-free defined medium to examine the expression of IPO13 and K17. Lentivirus-mediated silencing and overexpression IPO13 testing was conducted, and K17 alternation was evaluated with western blot and immunostaining. In addition, the translocation of c-Jun (a K17 regulator) was further examined after IPO13 was silenced. RESULTSIPO13 activity was significantly increased in the basal layer of the epithelium of the pterygium. In cultured PECs, overexpression or knockdown of the IPO13 gene increased or decreased PEC proliferation, respectively. IPO13 was colocalized with K17 in the epithelium of the pterygium, and overexpression or knockdown of the IPO13 gene induced upregulation or downregulation of K17 expression in PECs, respectively. In addition, silencing of the IPO13 gene blocked nuclear translocation of c-Jun. CONCLUSIONSWe provided novel evidence that IPO13 may contribute to the pathogenesis of pterygium via modulation of K17 and c-Jun.
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titleIncreased importin 13 activity is associated with the pathogenesis of pterygium.
descriptionPURPOSEWe previously reported that importin 13 (IPO13), a member of the importin-β family of nuclear import proteins, regulates nuclear import of the glucocorticoid receptor in airway epithelial cells, IPO13 serves as a potential marker for corneal epithelial progenitor cells, and IPO13 is associated with corneal cell proliferation. Here we investigated the role of IPO13 in the pathogenesis of pterygium and the underlying mechanism including interaction with other cell proliferation-related factors: keratin 17 (K17), a lesional protein and a member of the type I keratins, and c-Jun, a protein of the activator protein-1 complex. METHODSTissue samples were collected from primary pterygia, recurrent pterygia, and normal conjunctiva to perform the following experiments: immunohistochemical measurement of IPO13 and K17. Pterygium epithelial cells (PECs) were cultured in keratinocyte serum-free defined medium to examine the expression of IPO13 and K17. Lentivirus-mediated silencing and overexpression IPO13 testing was conducted, and K17 alternation was evaluated with western blot and immunostaining. In addition, the translocation of c-Jun (a K17 regulator) was further examined after IPO13 was silenced. RESULTSIPO13 activity was significantly increased in the basal layer of the epithelium of the pterygium. In cultured PECs, overexpression or knockdown of the IPO13 gene increased or decreased PEC proliferation, respectively. IPO13 was colocalized with K17 in the epithelium of the pterygium, and overexpression or knockdown of the IPO13 gene induced upregulation or downregulation of K17 expression in PECs, respectively. In addition, silencing of the IPO13 gene blocked nuclear translocation of c-Jun. CONCLUSIONSWe provided novel evidence that IPO13 may contribute to the pathogenesis of pterygium via modulation of K17 and c-Jun.
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titleIncreased importin 13 activity is associated with the pathogenesis of pterygium.
authorXu, Ke ; Tao, Tao ; Jie, Jing ; Lu, Xiaodong ; Li, Xuezhi ; Mehmood, Muhammad Aamer ; He, Hui ; Liu, Zhen ; Xiao, Xinye ; Yang, Jie ; Ma, Jian-Xing ; Li, Wei ; Zhou, Yueping ; Liu, Zuguo
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abstractPURPOSEWe previously reported that importin 13 (IPO13), a member of the importin-β family of nuclear import proteins, regulates nuclear import of the glucocorticoid receptor in airway epithelial cells, IPO13 serves as a potential marker for corneal epithelial progenitor cells, and IPO13 is associated with corneal cell proliferation. Here we investigated the role of IPO13 in the pathogenesis of pterygium and the underlying mechanism including interaction with other cell proliferation-related factors: keratin 17 (K17), a lesional protein and a member of the type I keratins, and c-Jun, a protein of the activator protein-1 complex. METHODSTissue samples were collected from primary pterygia, recurrent pterygia, and normal conjunctiva to perform the following experiments: immunohistochemical measurement of IPO13 and K17. Pterygium epithelial cells (PECs) were cultured in keratinocyte serum-free defined medium to examine the expression of IPO13 and K17. Lentivirus-mediated silencing and overexpression IPO13 testing was conducted, and K17 alternation was evaluated with western blot and immunostaining. In addition, the translocation of c-Jun (a K17 regulator) was further examined after IPO13 was silenced. RESULTSIPO13 activity was significantly increased in the basal layer of the epithelium of the pterygium. In cultured PECs, overexpression or knockdown of the IPO13 gene increased or decreased PEC proliferation, respectively. IPO13 was colocalized with K17 in the epithelium of the pterygium, and overexpression or knockdown of the IPO13 gene induced upregulation or downregulation of K17 expression in PECs, respectively. In addition, silencing of the IPO13 gene blocked nuclear translocation of c-Jun. CONCLUSIONSWe provided novel evidence that IPO13 may contribute to the pathogenesis of pterygium via modulation of K17 and c-Jun.
urlhttp://search.proquest.com/docview/1324390899/
date2013-01-01