Ischemic injury leads to extracellular matrix alterations in retina and optic nerve

Sci Rep. 2017 Mar 6;7:43470. doi: 10.1038/srep43470.


Retinal ischemia occurs in a variety of eye diseases. Restrained blood flow induces retinal damage, which leads to progressive optic nerve degeneration and vision loss. Previous studies indicate that extracellular matrix (ECM) constituents play an important role in complex tissues, such as retina and optic nerve. They have great impact on de- and regeneration processes and represent major candidates of central nervous system glial scar formation. Nevertheless, the importance of the ECM during ischemic retina and optic nerve neurodegeneration is not fully understood yet. In this study, we analyzed remodeling of the extracellular glycoproteins fibronectin, laminin, tenascin-C and tenascin-R and the chondroitin sulfate proteoglycans (CSPGs) aggrecan, brevican and phosphacan/RPTPβ/ζ in retinae and optic nerves of an ischemia/reperfusion rat model via quantitative real-time PCR, immunohistochemistry and Western blot. A variety of ECM constituents were dysregulated in the retina and optic nerve after ischemia. Regarding fibronectin, significantly elevated mRNA and protein levels were observed in the retina following ischemia, while laminin and tenascin-C showed enhanced immunoreactivity in the optic nerve after ischemia. Interestingly, CSPGs displayed significantly increased expression levels in the optic nerve. Our study demonstrates a dynamic expression of ECM molecules following retinal ischemia, which strengthens their regulatory role during neurodegeneration.

MeSH terms

  • Aggrecans / genetics
  • Aggrecans / metabolism
  • Animals
  • Brevican / genetics
  • Brevican / metabolism
  • Disease Models, Animal
  • Fibronectins / genetics
  • Fibronectins / metabolism
  • Gene Expression Regulation*
  • Laminin / genetics
  • Laminin / metabolism
  • Male
  • Optic Nerve / blood supply
  • Optic Nerve / metabolism*
  • Optic Nerve / pathology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Receptor-Like Protein Tyrosine Phosphatases, Class 5 / genetics
  • Receptor-Like Protein Tyrosine Phosphatases, Class 5 / metabolism
  • Reperfusion Injury / genetics*
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology
  • Retina / metabolism*
  • Retina / pathology
  • Retinal Degeneration / genetics*
  • Retinal Degeneration / metabolism
  • Retinal Degeneration / pathology
  • Signal Transduction
  • Tenascin / genetics
  • Tenascin / metabolism


  • Aggrecans
  • Bcan protein, rat
  • Brevican
  • Fibronectins
  • Laminin
  • RNA, Messenger
  • Tenascin
  • tenascin R
  • Receptor-Like Protein Tyrosine Phosphatases, Class 5