April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Protein Profile of Autosomal Recessive Congenital Hereditary Endothelial Dystrophy (CHED2) and Fuchs Endothelial Corneal dystrophy (FECD)
Author Affiliations & Notes
  • B. Hemadevi
    Department of Genetics, Dr.G.Venkataswamy Eye Research Institute, AMRF, Aravind Eye Hospital, Madurai, India
  • P. Sundaresan
    Department of Genetics, Dr.G.Venkataswamy Eye Research Institute, AMRF, Aravind Eye Hospital, Madurai, India
  • S. Ananthi
    Department of Genetics, Dr.G.Venkataswamy Eye Research Institute, AMRF, Aravind Eye Hospital, Madurai, India
  • M. Srinivasan
    Cornea services, Aravind Eye Hospital, Madurai, India
  • J. Arunkumar
    Cornea services, Aravind Eye Hospital, Madurai, India
  • N. V. Prajna
    Cornea services, Aravind Eye Hospital, Madurai, India
  • K. Dharmalingam
    Department of Genetic Engineering, Madurai Kamaraj University, Madurai, India
  • Footnotes
    Commercial Relationships  B. Hemadevi, None; P. Sundaresan, None; S. Ananthi, None; M. Srinivasan, None; J. Arunkumar, None; N.V. Prajna, None; K. Dharmalingam, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 4638. doi:
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      B. Hemadevi, P. Sundaresan, S. Ananthi, M. Srinivasan, J. Arunkumar, N. V. Prajna, K. Dharmalingam; Protein Profile of Autosomal Recessive Congenital Hereditary Endothelial Dystrophy (CHED2) and Fuchs Endothelial Corneal dystrophy (FECD). Invest. Ophthalmol. Vis. Sci. 2010;51(13):4638.

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

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Abstract

Purpose: : To examine the proteome with changes in corneal endothelial dystrophies CHED2 & FECD

Methods: : The study protocol had the approval of Institutional Review Board of Aravind eye hospital. Dystrophic corneas were collected from the patients during Penetrating Keratoplasty. Control corneas were obtained from Rotary Aravind International Eye Bank. Tissues were frozen in LQN2 and homogenized in ice using lysis buffer and the amount of protein was determined. Same concentration of proteins from each dystrophy and control corneas were subjected to 2-D analysis followed by nano LC-MS/MS. Experimental and biological replicates were carried out.

Results: : From the 2-D gels we observed nearly 120 individual spots from each group. We could perceive some differentially expressed spots between dystrophy and control gels and also between CHED2 and FECD. Ten different corneal proteins were identified through nano LC-MS/MS. Tentatively 65 proteins could be identified by matching the spots with the cornea 2D-PAGE database. There were marked differences on some of the proteins of blood/plasma, immune defense and antioxidant functional group. Interestingly we observed a spot from CHED2 which was present neither in control nor in FECD.

Conclusions: : This is the first study analyzing proteome of whole corneal tissue of CHED2 and FECD. The recognized unique spot present in CHED2 and up regulation or the down regulation of the specific proteins has to be analyzed further. The proteomic approach will provide better understanding and identification of the underlying genetic defects of these dystrophies.

Keywords: cornea: basic science • proteomics • degenerations/dystrophies 
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