TY - JOUR
T1 - Effect of the renin inhibitor aliskiren against retinal ischemia-reperfusion injury
AU - Tenkumo, Kaori
AU - Hirooka, Kazuyuki
AU - Sherajee, Shamshad J.
AU - Nakamura, Takehiro
AU - Itano, Toshifumi
AU - Nitta, Eri
AU - Fujita, Tomoyoshi
AU - Nishiyama, Akira
AU - Shiraga, Fumio
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2014/5
Y1 - 2014/5
N2 - The purpose of this study was to investigate the effect of the renin inhibitor, aliskiren, on retinal ischemia-reperfusion injury. Retinal ischemia was induced by increasing intraocular pressure to 130mmHg. At 7 days after ischemia, retinal damage was evaluated by measuring the retinal thickness and the number of retinal ganglion cells. Western blot was used to measure changes in the (pro)renin receptor expression. Retinal mRNA expressions of prorenin, angiotensinogen and angiotensin II type 1 receptor (AT1-R) were measured by real-time polymerase chain reaction. Rats were treated with the renin inhibitor, aliskiren. Although the number of retinal ganglion cells and the inner retinal thickness were significantly decreased at 7 days after ischemia, treatment with aliskiren significantly inhibited retinal ischemic injury. Administration of aliskiren increased mRNA expression of prorenin in the retina at 3h after the reperfusion. The expression of the (pro)renin receptor was not changed after ischemia-reperfusion injury with or without aliskiren. Although there was an increase in the retinal expression of AT1-R at 3h after the reperfusion, aliskiren administration suppressed this expression. A renin inhibitor attenuated subsequent ischemic damage in the rat retina via the inhibition of the prorenin-induced angiotensin generation.
AB - The purpose of this study was to investigate the effect of the renin inhibitor, aliskiren, on retinal ischemia-reperfusion injury. Retinal ischemia was induced by increasing intraocular pressure to 130mmHg. At 7 days after ischemia, retinal damage was evaluated by measuring the retinal thickness and the number of retinal ganglion cells. Western blot was used to measure changes in the (pro)renin receptor expression. Retinal mRNA expressions of prorenin, angiotensinogen and angiotensin II type 1 receptor (AT1-R) were measured by real-time polymerase chain reaction. Rats were treated with the renin inhibitor, aliskiren. Although the number of retinal ganglion cells and the inner retinal thickness were significantly decreased at 7 days after ischemia, treatment with aliskiren significantly inhibited retinal ischemic injury. Administration of aliskiren increased mRNA expression of prorenin in the retina at 3h after the reperfusion. The expression of the (pro)renin receptor was not changed after ischemia-reperfusion injury with or without aliskiren. Although there was an increase in the retinal expression of AT1-R at 3h after the reperfusion, aliskiren administration suppressed this expression. A renin inhibitor attenuated subsequent ischemic damage in the rat retina via the inhibition of the prorenin-induced angiotensin generation.
KW - (pro)renin
KW - Aliskiren
KW - Angiotensin II type 1 receptor (AT1-R)
KW - Angiotensinogen
KW - Renin
KW - Renin-angiotensin-aldosterone-system
KW - Retinal ischemia
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U2 - 10.1016/j.exer.2014.03.011
DO - 10.1016/j.exer.2014.03.011
M3 - Article
C2 - 24709336
AN - SCOPUS:84898681109
SN - 0014-4835
VL - 122
SP - 110
EP - 118
JO - Experimental Eye Research
JF - Experimental Eye Research
ER -