September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Corneal stromal tissue regeneration by stromal-derived stem cells
Author Affiliations & Notes
  • James L Funderburgh
    Univ of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States
  • Footnotes
    Commercial Relationships   James Funderburgh, None
  • Footnotes
    Support  NIH EY016415, DOD W81XWH-14-1-0465
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      James L Funderburgh; Corneal stromal tissue regeneration by stromal-derived stem cells. Invest. Ophthalmol. Vis. Sci. 201657(12):.

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

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Presentation Description : The limbal stroma contains a rare population of mesenchymal stem cells immediately subjacent to the epithelial basement membrane. These cells have been termed ‘niche cells’ because they exhibit direct contact with limbal epithelial stem cells and help maintain the LSC phenotype in vitro. The niche cells, when isolated and expanded in culture, exhibit properties of adult stem cells. Our work has shown these corneal stromal stem cells (CSSC) express genes typical of mesenchymal and embryonic stem cells as well as gene products present in neural crest cells and during ocular development. CSSC can be expanded >107 fold before senescence, providing an abundant resource for regenerative applications. When injected into the stroma of a lumican knockout mouse, human CSSC initiate tissue remodeling bringing matrix organization and transparency to the corneas. When CSSC are layered over a stromal debridement wound, fibrotic scar tissue is not deposited rather the ablated tissue is regenerated with matrix indistinguishable the original. This regenerative ability is accompanied by immune-suppressive properties of the CSSC. In vivo, neutrophil infiltration is suppressed after wounding and human CSSC do not elicit T-cell mediated rejection in mouse corneas. In vitro, CSSC block T-cell activation and proliferation. They also modify macrophage phenotype and expression of TGF betas, important mediators of fibrosis. These results implicate the regenerative properties of CSSC with their effect on the immune response of the host. Our current work focuses on the mechanism by which the CSSC exert these effects.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.


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