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Author Notes:

Correspondence and requests for materials should be addressed to Y.D. (email: duy@upmc.edu)

These authors contributed equally: Hongmin Yun, Yiwen Wang, Yi Zhou.

H.Y., Y.W., Y.Z., and Y.D. designed research; H.Y., Y.W., Y.Z., K.W., M.S., and Y.D. performed research; H.Y., Y.W., Y.Z., K.W., M.S., D.B.S., X.X., C.R.E., and Y.D. analyzed the data; and H.Y., Y.W., Y.Z., C.R.E., and Y.D. wrote the paper.

We thank Dr. Andrew Hertsenberg for his critical review and editing of the manuscript and Ms. Yi Xu for her help with statistical analysis.

The authors declare no competing interests.


Research Funding:

The work was supported by NIH/NEI grants EY025643 (to Y.D.), EY019696 (to C.R.E.), P30-EY008098, BrightFocus Foundation G2014086 (to Y.D.); Eye and Ear Foundation (Pittsburgh, PA); Research to Prevent Blindness; Georgia Research Alliance (to C.R.E.); and an anonymous philanthropic donation (to Y.D.).


  • Glaucoma
  • Mesenchymal stem cells
  • Ophthalmology
  • Regeneration

Human stem cells home to and repair laser-damaged trabecular meshwork in a mouse model.

Journal Title:

Communications Biology


Volume 1


, Pages 216-216

Type of Work:

Article | Final Publisher PDF


Glaucoma is the leading cause of irreversible vision loss, and reducing elevated intraocular pressure is currently the only effective clinical treatment. The trabecular meshwork is the main resistance site for aqueous outflow that maintains intraocular pressure. In this study, we transplanted human trabecular meshwork stem cells (TMSCs) intracamerally into mice that received laser photocoagulation over a 180° arc of the trabecular meshwork. TMSCs preferentially homed and integrated to the laser-damaged trabecular meshwork region and expressed differentiated cell markers at 2 and 4 weeks. Laser-induced inflammatory and fibrotic responses were prevented by TMSC transplantation with simultaneous ultrastructure and function restoration. Cell affinity and migration assays and elevated expression of CXCR4 and SDF1 in laser-treated mouse trabecular meshwork suggest that the CXCR4/SDF1 chemokine axis plays an important role in TMSC homing. Our results suggest that TMSCs may be a viable candidate for trabecular meshwork refunctionalization as a novel treatment for glaucoma.

Copyright information:

© The Author(s) 2018

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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