June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Proliferation potential of Müller glia after retinal damage varies between mouse strains
Author Affiliations & Notes
  • Akiko Suga
    National Institute of Sensory Organs, Tokyo Medical Center, Tokyo, Japan
  • Kazuyo Sadamoto
    CDB, RIKEN, Kobe, Japan
  • Momo Fujii
    CDB, RIKEN, Kobe, Japan
  • Michiko Mandai
    CDB, RIKEN, Kobe, Japan
  • Masayo Takahashi
    CDB, RIKEN, Kobe, Japan
  • Takeshi Iwata
    National Institute of Sensory Organs, Tokyo Medical Center, Tokyo, Japan
  • Footnotes
    Commercial Relationships Akiko Suga, None; Kazuyo Sadamoto, None; Momo Fujii, None; Michiko Mandai, None; Masayo Takahashi, None; Takeshi Iwata, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 5496. doi:
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    • Get Citation

      Akiko Suga, Kazuyo Sadamoto, Momo Fujii, Michiko Mandai, Masayo Takahashi, Takeshi Iwata; Proliferation potential of Müller glia after retinal damage varies between mouse strains. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5496.

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

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Abstract

Purpose: Retinal Müller glia can serve as a source to regenerate retinal neurons after damage in vertebrates, however, this regeneration is strictly limited in rodents. We tested whether Müller glial response after retinal damage varied between mouse strains, and examined the difference of gene expression levels between the mouse strains.

Methods: Retinal explant culture was used as a model to induce cell death preferentially in the photoreceptor cells. Retinal explants were made from 9-10 weeks postnatal male C57 BL/6 (B6) (N=4), BDF1 (N=5), and 129X1/SvJ (129) (N=6) mice, and cultured for 4 days with or without GSK3 inhibitor. The retinal explants were fixed and stained with BrdU, Pax6 and Chx10, and Cyclin D families to compare the number of Müller glia which entered into cell cycle between mouse strains. Total RNA was extracted from B6 and 129 normal retinas and retinal explants cultured for 3 days, and processed for microarray analyses. Transcripts with significant difference in the expression levels between B6 and 129 were statistically identified and further classified according to the functional categories.

Results: Larger numbers of proliferative Müller glia indicated by BrdU-incorporation were detected in the retinal explants from 129 and BDF1 compared with B6. The number of proliferative Müller glia was remarkably increased by the addition of GSK3 inhibitor in 129 and BDF1, but not in B6. Müller glia expressed CyclinD1 in both 129 and B6, but Ki67-positive Müller glia was detected only in 129. Retinal progenitor-like cells positive for Pax6 and Chx10 were detected both in 129 and B6, but their localization in the retina was different. Gene expression analyses suggested that retinal progenitor genes were upregulated in 129 after damage, on the other hand, genes related to inflammatory response were higher in B6. Two chromatin-binding factors with distinct functions were differentially expressed in 129 and B6 after retinal damage, respectively.

Conclusions: The response of Müller glia after damage varied between mouse strains in the degree of proliferation and response to growth factors. Consistent with the hypothesis that Müller glia changed to retinal progenitor-like state and proliferated, retinal progenitor genes were upregulated in the retina with more proliferative Müller glia, however, genes related to inflammatory response were higher in the retina with less proliferative Müller glia.

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