Contribution of Calpain and Caspases to Cell Death in Cultured Monkey RPE Cells | Zendy

Emi Nakajima | Zendy; Katherine B. Hammond | Zendy; Masayuki Hirata | Zendy; Thomas R. Shearer | Zendy; Mitsuyoshi Azuma | Zendy

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Contribution of Calpain and Caspases to Cell Death in Cultured Monkey RPE Cells

Author(s) -

Emi Nakajima,

Katherine B. Hammond,

Masayuki Hirata,

Thomas R. Shearer,

Mitsuyoshi Azuma

Publication year - 2017

Publication title -

investigative ophthalmology and visual science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.935

H-Index - 218

eISSN - 1552-5783

pISSN - 0146-0404

DOI - 10.1167/iovs.17-22325

Subject(s) - calpain , caspase , apoptosis , proteases , programmed cell death , microbiology and biotechnology , caspase 3 , hypoxia (environmental) , biology , chemistry , biochemistry , enzyme , organic chemistry , oxygen

AMD is the leading cause of human vision loss after 65 years of age. Several mechanisms have been proposed: (1) age-related failure of the choroidal vasculature leads to loss of RPE; (2) RPE dysfunctions due to accumulation of phagocytized, but unreleased A2E (N-retinylidene-N-retinylethanolamine); (3) zinc deficiency activation of calpain and caspase proteases, leading to cell death. The purpose of the present study is to compare activation of calpain and caspase in monkey RPE cells cultured under hypoxia or with A2E.

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