May 2003
Volume 44, Issue 13
ARVO Annual Meeting Abstract  |   May 2003
Müller Cell Adhesion in Tractional Force Generation
Author Affiliations & Notes
  • K.M. Bradley
    Ophthalmology, Univ of Alabama at Birmingham, Birmingham, AL, United States
  • C. Guidry
    Ophthalmology, Univ of Alabama at Birmingham, Birmingham, AL, United States
  • Footnotes
    Commercial Relationships  K.M. Bradley, None; C. Guidry, None.
  • Footnotes
    Support  Juvenile Diabetes Research Foundation, NIH EY13258
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 2955. doi:
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      K.M. Bradley, C. Guidry; Müller Cell Adhesion in Tractional Force Generation . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2955.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: Müller cells, the principal glia of the retina, are involved in fibroproliferative ocular diseases such as proliferative diabetic retinopathy and are capable of generating tractional forces in response to IGF-I and IGF-II. As tractional forces result from extracellular matrix contraction by cells, mechanistic studies of this activity are of immediate relevance to the pathogenesis of fibroproliferative disorders complicated by traction retinal detachment. The present study tests the hypothesis that cell adhesion to deformable matrices and, thus tractional force generation, involves a fundamentally different mechanism from that classically described for focal adhesion formation. Methods: Extracellular matrix contraction was examined using an established culture model involving incubation of insulin-like growth factor I-stimulated porcine Müller cells on gels formed with native type I collagen. Recruitment and localization of focal adhesion proteins were examined by Western blotting and indirect immunofluorescent localization with monoclonal antibodies raised against alpha-actinin, focal adhesion kinase, paxillin, talin, tensin, vinculin and the beta 1 integrin subunit. Results: Müller cell adhesion to fibronectin- or collagen-coated cover slips (non-deformable substrata) resulted in similar rates of cell spreading, beta 1 integrin-positive focal adhesion formation and development of actin-positive stress fibers. All six focal adhesion proteins could be localized to focal adhesions formed under these circumstances and recruitment to a nonionic detergent insoluble pool was detected in Western blots. In contrast, Müller cells adhering to collagen gels for the same period developed a stellate morphology and lacked stress fibers as well as beta 1 integrin or focal adhesion protein aggregates. Of the proteins examined, only beta-1 integrin and tensin were recruited to the nonionic detergent insoluble pool. Conclusions: Müller cell adhesion to deformable collagen gels, compared to non-deformable collagen-coated cover slips, differs with respect to cell morphology, actin stress fiber formation, and recruitment of focal adhesion proteins. We conclude that Müller cell adhesion to and contraction of deformable collagen substrata involves a fundamentally different adhesion mechanism from that classically described for the formation of focal adhesions.

Keywords: cell adhesions/cell junctions • Muller cells • retinal detachment 

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