Atoh7 promotes retinal Müller cell differentiation into retinal ganglion cells.

Cytotechnology

State Key Lab of Medical Genetics of China, Central South University, Changsha, China.

Published: March 2016

AI Article Synopsis

  • Glaucoma leads to the death of retinal ganglion cells, making it a major eye disease concern.
  • Researchers found that retinal Müller cells can act like stem cells and, under certain conditions, can turn into ganglion cells, but current methods don't provide enough cells for treatment.
  • The study introduced the gene Atoh7 into dedifferentiated retinal Müller cells, resulting in a significantly higher number of ganglion cells, suggesting Atoh7 could be a key to gene therapy for glaucoma and optic nerve regeneration.

Article Abstract

Glaucoma is one of the leading eye diseases due to the death of retinal ganglion cells. Increasing evidence suggests that retinal Müller cells exhibit the characteristics of retinal progenitor cells and can differentiate to neurons in injured retinas under certain conditions. However, the number of ganglion cells differentiated from retinal Müller cells falls far short of therapeutic needs. This study aimed to promote the differentiation of retinal Müller cells into ganglion cells by introducing Atoh7 into the stem cells dedifferentiated from retinal Müller cells. Rat retinal Müller cells were isolated and dedifferentiated into stem cells, which were transfected with PEGFP-N1 or PEGFP-N1-Atoh7 vector, and then further induced to differentiate into ganglion cells. The proportion of ganglion cells differentiated from Atoh7-tranfected stem cells was significantly higher than that of control transfected or untransfected cells. In summary, Atoh7 promotes the differentiation of retinal Müller cells into retinal ganglion cells. This may open a new avenue for gene therapy of glaucoma by promoting optic nerve regeneration.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4754246PMC
http://dx.doi.org/10.1007/s10616-014-9777-1DOI Listing

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