April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
A Subpopulation of Skeletal Muscle Stem Cells Can Cause Lens Fibrotic Disease
Author Affiliations & Notes
  • J. L. Walker
    Pathology/Anatomy&Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania
  • L. Zhang
    Pathology/Anatomy&Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania
  • I. Wolff
    Pathology/Anatomy&Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania
  • J. Gerhart
    Lankenau Medical Research Institute, Wynnewood, Pennsylvania
  • M. George-Weinstein
    Lankenau Medical Research Institute, Wynnewood, Pennsylvania
  • A. Menko
    Pathology/Anatomy&Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania
  • Footnotes
    Commercial Relationships  J.L. Walker, Thomas Jefferson University, P; L. Zhang, None; I. Wolff, None; J. Gerhart, Lankenau Medical Research Institute, P; M. George-Weinstein, Lankenau Medical Research Institute, P; A. Menko, Thomas Jefferson University, P.
  • Footnotes
    Support  EY014798, EY010577, EY014258
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 4768. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      J. L. Walker, L. Zhang, I. Wolff, J. Gerhart, M. George-Weinstein, A. Menko; A Subpopulation of Skeletal Muscle Stem Cells Can Cause Lens Fibrotic Disease. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4768.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : The acquisition of a myofibroblast phenotype causes the lens fibrotic disease Posterior Capsule Opacification (PCO). Although the appearance of myofibroblasts is thought to result from an epithelial to mesenchymal transition, the cells which give rise to myofibroblasts and the etiology of PCO disease are unknown. Using an ex vivo lens fibrotic disease model that recapitulates the major features of PCO, including proliferation, migration and expression of mesenchymal markers, we investigated the identity of the cell population responsible for causing lens fibrotic disease. These studies focused on a possible role for skeletal muscle stem cells (skm stem cells), a newly identified population of cells in the lens that express MyoD mRNA and the G8 antigen.

Methods: : After mock cataract surgery, chick lens capsular bags were pinned to a culture dish as previously described. G8 positive (G8+)/MyoD expressing skm cells were identified by immunolocalization and in situ hybridization. G8+ cells in the ex vivo cultures were ablated by incubation with G8 antibody followed by complement. Expression of the mesenchymal marker -smooth muscle actin (-SMA) was determined by Western blot analysis.

Results: : Subpopulations of skm stem cells were identified in niches nestled among the cells of the equatorial zone of the lens. This discovery identified for the first time a cell population in the lens epithelium not derived from the lens epithelial cell. Following mock cataract surgery, the skm cells activated by the wounding emerged from their niches and migrated to the leading edge of the lens epithelial cell monolayer. Ablation of the skm cells blocked the appearance of mesenchymal cells as defined by inhibition of -SMA expression.

Conclusions: : Injury associated with mock cataract surgery activates a unique population of skm stem cells, causing them to emerge from their niches to participate in wound healing by migrating to the leading edge of the collectively migrating lens epithelial cell sheet. However, these cells are also responsible for the appearance of -SMA-expressing myofibroblasts in the PCO culture model. These results suggest that the skm stem cells are a cause of lens fibrotic disease.

Keywords: posterior capsular opacification (PCO) • EMT (epithelial mesenchymal transition) 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×