March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
The Kinetics of Retinal Gene Expression Profile of Ccl2/Cx3cr1 Double Deficient Mice on rd8 Background
Author Affiliations & Notes
  • De Fen Shen
    Laboratory of Immunology, National Eye Inst/NIH, Bethesda, Maryland
  • Yujuan Wang
    Laboratory of Immunology, National Eye Inst/NIH, Bethesda, Maryland
  • Kangxin Jin
    Center for Advanced Biotechnology and Medicine, University of Medicine and Dentistry of New Jersey, Piscataway, New Jersey
  • Jingsheng Tuo
    Laboratory of Immunology, National Eye Inst/NIH, Bethesda, Maryland
  • Mengqing Xiang
    Center for Advanced Biotechnology and Medicine, University of Medicine and Dentistry of New Jersey, Piscataway, New Jersey
  • Chi-Chao Chan
    Laboratory of Immunology, National Eye Inst/NIH, Bethesda, Maryland
  • Footnotes
    Commercial Relationships  De Fen Shen, None; Yujuan Wang, None; Kangxin Jin, None; Jingsheng Tuo, None; Mengqing Xiang, None; Chi-Chao Chan, None
  • Footnotes
    Support  NEI Intramural Research Program
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 6495. doi:
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      De Fen Shen, Yujuan Wang, Kangxin Jin, Jingsheng Tuo, Mengqing Xiang, Chi-Chao Chan; The Kinetics of Retinal Gene Expression Profile of Ccl2/Cx3cr1 Double Deficient Mice on rd8 Background. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6495.

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

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Abstract

Purpose: : Ccl2/Cx3cr1double deficient mouse on rd8 background (DKO) develops focal age-related macular degeneration (AMD)-like retinal lesions with photoreceptor and RPE degeneration, elevated A2E, microglial activation, and occasional chorioretinal neovascularization progressing with age. To further understand the mechanism in the retinal lesion, we performed the microarray to investigate retinal gene expression profile in DKO in comparison with wild type (WT). The differentially expressed genes were further determined in their expression at different age, and compared with parental mice, Ccl2-/- and Cx3cr1-/-.

Methods: : Funduscopy was performed for each mouse before euthanization. RNA isolated from 4 month old DKO and WT mouse retina was used for microarray. The confirmation RT-PCR of glial fibrillary acidic protein (Gfap), N-terminal EF-hand calcium binding protein (Necab1), Keratin 13 (Krt13), chemokine (C-C motif) ligand 21A (Ccl21a), neuron specific gene family member 2 (Nsg2), matrix metallopeptidase 15 (Mmp15), retinol binding protein 3 (Rbp3), chloride channel calcium activated 5 (Clca5) and tyrosinase-related protein 1 (Tyrp1) genes was performed for RNA isolation from different age of DKO, WT, Ccl2-/- and Cx3cr1-/- mouse retina.

Conclusions: : Increase of Gfap, a glia specific marker and one of the earliest indicators of retinal damage, companied with increases of nerve tissue damage markers, Necab1and Nsg2, and reduce of retinol binding protein, Rbp3, correlated with the progression of retinal degeneration in DKO and Ccl2-/-, especially in DKO. The results suggested that retinal gliosis could play a role in aging and AMD development.

Keywords: gene microarray • aging • glia 
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