Document Detail


Conditional deletion of beta1-integrin from the developing lens leads to loss of the lens epithelial phenotype.
MedLine Citation:
PMID:  17493607     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Beta1-integrins are cell surface receptors that participate in sensing the cell's external environment. We used the Cre-lox system to delete beta1-integrin in all lens cells as the lens vesicle transitions into the lens. Adult mice lacking beta1-integrin in the lens are microphthalmic due to apoptosis of the lens epithelium and neonatal disintegration of the lens fibers. The first morphological alterations in beta1-integrin null lenses are seen at 16.5 dpc when the epithelium becomes disorganized and begins to upregulate the fiber cell markers beta- and gamma-crystallins, the transcription factors cMaf and Prox1 and downregulate Pax6 levels demonstrating that beta1-integrin is essential to maintain the lens epithelial phenotype. Furthermore, beta1-integrin null lens epithelial cells upregulate the expression of alpha-smooth muscle actin and nuclear Smad4 and downregulate Smad6 suggesting that beta1-integrin may brake TGFbeta family signaling leading to epithelial-mesenchymal transitions in the lens. In contrast, beta1-integrin null lens epithelial cells show increased E-cadherin immunoreactivity which supports the proposed role of beta1-integrins in mediating complete EMT in response to TGFbeta family members. Thus, beta1-integrin is required to maintain the lens epithelial phenotype and block inappropriate activation of some aspects of the lens fiber cell differentiation program.
Authors:
Vladimir N Simirskii; Yan Wang; Melinda K Duncan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2007-04-12
Journal Detail:
Title:  Developmental biology     Volume:  306     ISSN:  0012-1606     ISO Abbreviation:  Dev. Biol.     Publication Date:  2007 Jun 
Date Detail:
Created Date:  2007-06-11     Completed Date:  2007-08-01     Revised Date:  2014-09-15    
Medline Journal Info:
Nlm Unique ID:  0372762     Medline TA:  Dev Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  658-68     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD29 / genetics*
Apoptosis
Cell Proliferation
Crystallins / metabolism
Epithelium / embryology*,  metabolism
Gene Deletion*
Homozygote
Immunohistochemistry
In Situ Nick-End Labeling
Lens, Crystalline / embryology*
Mesoderm / metabolism
Mice
Mice, Transgenic
Phenotype
Grant Support
ID/Acronym/Agency:
EY 015279/EY/NEI NIH HHS; P20 RR 16472/RR/NCRR NIH HHS; R01 EY015279/EY/NEI NIH HHS; R01 EY015279-03/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD29; 0/Crystallins
Comments/Corrections

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