Changes in rhodopsin kinase and transducin in the rat retina in early-stage diabetes

被引:23
|
作者
Kim, YH
Kim, YS
Noh, HS
Kang, SS
Cheon, EW
Park, SK
Lee, BJ
Choi, WS
Cho, GJ
机构
[1] Gyeongsang Natl Univ, Coll Med, Inst Hlth Sci, Dept Anat & Neurobiol, Jinju 660751, Gyungnam, South Korea
[2] Jinju Int Univ, Dept Food Sci, Jinju 660845, Gyungnam, South Korea
[3] Univ Ulsan, Coll Med, Dept Pediat, Ulsan 682060, South Korea
[4] Univ Ulsan, Coll Nat Sci, Dept Biol Sci, Ulsan 680749, South Korea
关键词
rhodopsin kinase; transducin-alpha (G(t alpha)); recoverin; phototransduction; streptozotocin; retina;
D O I
10.1016/j.exer.2004.09.003
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
To establish changes in phototransduction in diabetes, the effects of high glucose on rhodopsin kinase (RK) and transducin (G,), as well as recoverin, were examined in the retina of STZ-induced diabetic rats. Diabetes was induced by single intraperitoneal injection of STZ (50 mg/kg) to Sprague-Dawley (SD) rats and the animals were sacrificed after 6 weeks. Immunohistochemistry (IHC) and Western blot analysis were carried out using antibodies against RK and G(t alpha) (alpha subunit of G(t)) in the STZ-induced diabetic retina and the control retina. The expression level of recoverin protein was also analysed. In the diabetic retina, while the expression of RK protein increased, that of Gt, and recoverin proteins decreased. RK immunoreactivity (IR) appeared generally in the retina, and its signal increased in the outer limiting membrane (OLM), some rod cells in the outer segment layer (OSL) and at the tip of the outer plexiform layer (OPL) in the diabetic retina. G(t alpha)-IR also appeared in the OPL and in photoreceptor layer. In the diabetic retina, G(t alpha)-IR significantly decreased in the OPL, indicating RK-IR increase. This study illustrates the alterations in RK, G(t alpha) and recoverin in the diabetic retina that may induce dysfunctions in phototransduction even in early-stage diabetes. (c) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:753 / 760
页数:8
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