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Calpain involvement in monkey retinal cell damage due to hypoxia
Author(s) -
Nakajima Emi,
Shearer Thomas R.,
Azuma Mitsuyoshi
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.793.1
Subject(s) - calpain , retina , immunocytochemistry , microbiology and biotechnology , retinal , vimentin , biology , spectrin , glaucoma , cell , neuroscience , endocrinology , immunology , cytoskeleton , immunohistochemistry , biochemistry , enzyme
One of the leading causes of blindness is retinal damage caused by the high intraocular pressure (IOP) in glaucoma. Previous studies in rats have suggested that the proteolytic enzyme calpain was involved in ganglion cells death during ischemia and acute high IOP. Glial cells are thought to protect neurons from various insults. For example, Müller cells, one type of glial cell in retina, are known to rescue ganglion cells from glutamate and NO neurotoxicities. The purpose of the present study using primate retina was to explain the role of calpains in hypoxic Müller cells. When dissociated cells from monkey retina were cultured for two weeks, Müller cells were observed with fewer photoreceptor cells, as identified by immunocytochemistry using vimentin and rhodopsin as markers. Under hypoxia, both types of cells were damaged, and a calpain‐specific α‐spectrin breakdown product (SBDP) was detected by immunocytochemistry. Activation of calpains 1 and 2, SBDP production and vimentin degradation were also observed by immunoblotting in hypoxic cells. When SNJ‐1945 calpain inhibitor was included during hypoxic culture, all the above changes were inhibited. The recovery of Müller cell damage by SNJ‐1945 might have important implications regarding amelioration of ganglion cell damage in glaucoma patients. Dr. Shearer receives consulting fees from, and Dr. Azuma is an employee of, Senju Pharmaceutical Co. Ltd.