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Cytochemical alterations in the rat retina by LPS administration

Title
Cytochemical alterations in the rat retina by LPS administration
Authors
Jang S.Lee J.-H.Choi K.-R.Kim D.Yoo H.-S.Oh S.
Ewha Authors
최규룡오세관
SCOPUS Author ID
최규룡scopus; 오세관scopus
Issue Date
2007
Journal Title
Neurochemical Research
ISSN
0364-3190JCR Link
Citation
Neurochemical Research vol. 32, no. 1, pp. 1 - 10
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
LPS-induced inflammation and changes in protein phosphorylation and the JAK-STAT pathway accompanying glial activation after LPS treatment, were followed by analyzing secreted proinflammatory cytokine levels. The administration of LPS caused tyrosine phosphorylation of STAT3 in retinae and induced glial fibrillary acidic protein. (GFAP) from the nerve fiber layer to the ganglion cell layer. Our results suggest that the LPS-induced activation of the JAK2/STAT3 signaling pathway may play a key role in the induction of astrogliosis. However, no significant increase in vimentin, OX-42 or inducible nitric oxide synthase (iNOS) expressions were observed after LPS administration. Sphingosine kinase catalyzes the conversion of sphingosine to sphingosine-1-phosphate (So-1-P), a sphingolipid metabolite that plays important roles in angiogenesis, inflammation, and cell growth. In the present study, it was found that sphingolipid metabolite levels were elevated in the serum and retinae of LPS-injected rats. To further investigate the chronic effect of increased So-1-P in the retina, So-1-P was infused intracerebroventricularly (i.c.v.) into rats using an osmotic minipump at 100 pmol/10 μl h-1 for 7 days, and was found to increase retinal GFAP expression. These observations suggest that LPS induces the activation of retinal astrocytes via JAK2/STAT3 and that LPS affects So-1-P generation. Our findings also suggest that elevated So-1-P in the retina and/or in serum could induce cytochemical alterations in LPS treated or inflamed retinae. © 2006 Springer Science+Business Media, LLC.
DOI
10.1007/s11064-006-9215-7
Appears in Collections:
의과대학 > 의학과 > Journal papers
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