Retinal degeneration in transgenic mice induced by oncostatin M through gp130/OSMR? receptor
- VernacularTitle:制瘤素通过其受体gp130/OSMR?诱发转基因鼠视网膜变性
- Author:
Xiaobo XIA
;
Xia ZHOU
;
Huizhuo XU
- Publication Type:Journal Article
- Keywords:
Retinal degeneration;
Cytochrome C/immunology;
Mice, transgenic;
Interleukin-6;
Cell death/immunology
- From:
Chinese Journal of Ocular Fundus Diseases
2001;0(03):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To determine the signal pathway of specifically expressed oncostatin M(OSM) in lens inducing retinal degeneration in transgenic mice. Methods A sequence-truncated OSM cDNA (661 bp) of mice was linked to ?A-crytallin promoter, and was micro-injected into unicellular embryo to set up the model of transgenic mice. Reversal transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA expression of gp130/OSMR? receptor in the retinae of OSM transgenic and non-transgenic mice. Rabbit anti-phosphorylated STAT-3 antibody was used to detect the protein expression of phosphorylated STAT-3,and mouse anti-cytochrome C antibody was used to detect the distributing of cytochrome C in retinae. Results Expression of gp130/OSMR? mRNA was found in retina of non-transgenic mice. At the 17.5th day in the embryonic stage, significant accumulation of the phosphorylated STAT-3 was detected in the retinal nucleolus in OSM transgenic retina. At the first day after birth, intensive staining of cytochrome C in OSM transgenic retina was found. Conclusions specifically expressed OSM in lens may act on gp130/OSMR? receptor in retinae, activate STAT-3, and cause the release of cytochrome C from mitochondria, which eventually induces widespread retinal degeneration.
