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Investigative ophthalmology & visual science2011; 52(5); 2314-2320; doi: 10.1167/iovs.10-6475

Changes in matrix metalloproteinase network in a spontaneous autoimmune uveitis model.

Abstract: Autoimmune uveitis is a sight-threatening disease in which autoreactive T cells cross the blood-retinal barrier. Molecular mechanisms contributing to the loss of eye immune privilege in this autoimmune disease are not well understood. In this study, the authors investigated the changes in the matrix metalloproteinase network in spontaneous uveitis. Methods: Matrix metalloproteinase (MMP) MMP2, MMP9, and MMP14 expression and tissue inhibitor of metalloproteinase (TIMP)-2 and lipocalin 2 (LCN2) expression were analyzed using Western blot quantification. Enzyme activities were examined with zymography. Expression patterns of network candidates were revealed with immunohistochemistry, comparing physiological appearance and changes in a spontaneous recurrent uveitis model. Results: TIMP2 protein expression was found to be decreased in both the vitreous and the retina of a spontaneous model for autoimmune uveitis (equine recurrent uveitis [ERU]), and TIMP2 activity was significantly reduced in ERU vitreous. Functionally associated MMPs such as MMP2, MMP14, and MMP9 were found to show altered or shifted expression and activity. Although MMP2 decreased in ERU vitreous, MMP9 expression and activity were found to be increased. These changes were reflected by profound changes within uveitic target tissue, where TIMP2, MMP9, and MMP14 decreased in expression, whereas MMP2 displayed a shifted expression pattern. LCN2, a potential stabilizer of MMP9, was found prominently expressed in equine healthy retina and displayed notable changes in expression patterns accompanied by significant upregulation in autoimmune conditions. Invading cells expressed MMP9 and LCN2. Conclusions: This study implicates a dysregulation or a change in functional protein-protein interactions in this TIMP2-associated protein network, together with altered expression of functionally related MMPs.
Publication Date: 2011-04-08 PubMed ID: 21228380DOI: 10.1167/iovs.10-6475Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This research article analyzes the changes in the matrix metalloproteinase network in cases of autoimmune uveitis. It provides an insight, indicating a dysregulation or a shift in protein-protein interactions which could influence the progression of this sight-threatening disease.

Research Methodology

  • The researchers in this study employed a range of experimental techniques. They used Western blot quantification to analyze MMP2, MMP9, and MMP14 (matrix metalloproteinases) expressions along with tissue inhibitor of metalloproteinase-2 (TIMP-2) and lipocalin 2 (LCN2) expressions.
  • Zymography was used to examine enzyme activities that may have a significant role in the development of the disease.
  • Immunohistochemistry was utilized for revealing the expression patterns of network candidates, comparing physiological appearance and changes in a spontaneous recurrent uveitis model.

Experimental Findings

  • In the study, the authors observed a decrease in the TIMP2 protein expression in both the vitreous and retina of an autoimmune uveitis model named equine recurrent uveitis (ERU). The activity of TIMP2 was also noticed to have significantly reduced in ERU vitreous.
  • MMPs such as MMP2, MMP14, and MMP9 showed altered or shifted expression and activity. Whereas MMP2 decreased in ERU vitreous, MMP9’s expression and activity increased.
  • Changes were also noticeable within the uveitic target tissue. TIMP2, MMP9, and MMP14 decreased in expression, while MMP2 experienced a shift in its expression pattern.
  • LCN2, a likely stabilizer of MMP9, was found prominently in the healthy equine retina. It showed an upregulation in expression patterns under autoimmune conditions.
  • Invading cells were observed to express MMP9 and LCN2, potentially driving the development of uveitis.

Conclusions

  • The research implicates a dysregulation or a change in functional protein-protein interactions in this TIMP2-associated protein network. These changes, coupled with altered expression of functionally related MMPs, may significantly contribute to the pathogenesis of autoimmune uveitis.
  • The findings provide insights into the molecular mechanisms underlying autoimmune uveitis, which could allow the development of improved therapeutic strategies for this blinding disease.

Cite This Article

APA
Hofmaier F, Hauck SM, Amann B, Degroote RL, Deeg CA. (2011). Changes in matrix metalloproteinase network in a spontaneous autoimmune uveitis model. Invest Ophthalmol Vis Sci, 52(5), 2314-2320. https://doi.org/10.1167/iovs.10-6475

Publication

ISSN: 1552-5783
NlmUniqueID: 7703701
Country: United States
Language: English
Volume: 52
Issue: 5
Pages: 2314-2320

Researcher Affiliations

Hofmaier, Florian
  • Institute of Animal Physiology, Department of Veterinary Sciences, Faculty of Veterinary Medicine, Ludwig-Maximilians-University Munich, Munich, Germany.
Hauck, Stefanie M
    Amann, Barbara
      Degroote, Roxane L
        Deeg, Cornelia A

          MeSH Terms

          • Animals
          • Autoimmune Diseases / enzymology
          • Autoimmune Diseases / veterinary
          • Blotting, Western
          • Disease Models, Animal
          • Fluorescent Antibody Technique, Indirect
          • Horse Diseases / enzymology
          • Horses
          • Lipocalins / metabolism
          • Matrix Metalloproteinases / metabolism
          • Recurrence
          • Retina / enzymology
          • Tissue Inhibitor of Metalloproteinase-2 / metabolism
          • Uveitis / enzymology
          • Uveitis / veterinary
          • Vitreous Body / enzymology

          Citations

          This article has been cited 17 times.
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