Post-Translational Modification of Crystallins in Vitreous Body from Experimental Autoimmune Uveitis of Rats
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- 作者：Song-Chul Bahk ; Jung-Un Jang ; Chang-Uk Choi ; Sook-Hee Lee ; Zee-Yong Park ; Ji-Yeon Yang ;
; Jae-Duck Kim ; Yun-Sik Yang ; Hun-Taeg Chung - 刊名：Journal of Proteome Research
- 出版年：2007
- 出版时间：October 2007
- 年：2007
- 卷：6
- 期：10
- 页码：3891 - 3898
- 全文大小：812K
- 年卷期：v.6,no.10(October 2007)
- ISSN：1535-3907
文摘
Experimental autoimmune uveitis (EAU) is a well-known animal model of posterior uveitis that is oneof the major causes of blindness. EAU could be induced in susceptible animals (i.e., Lewis rat) byimmune reactions using evolutionarily conserved retinal proteins, such as interphoto-receptor retinoidbinding protein (IRBP), or epitaphs of the protein. First, we prepared the following four test groupsthat subsequently increased or decreased inflammation. (1) Normal control group, (2) IRBP-induceduveitis group, (3) Hemin-treated uveitis group, and (4) Sn(IV) protoporphyrin IX dichloride (SnPP)-treated uveitis group. Second, in the vitreous bodies of Lewis rats, the infiltrated proteins were analyzedusing two-dimensional electrophoresis (2-DE), MALDI-TOF/MS, and Micro LC/LC-MS/MS analysis.Finally, Western blotting was applied to confirm the relative amount of crystallins and phosphorylationsites of B-crystallin. Thirty spots were identified in vitreous bodies, and 27 of these spots were membersof the crystallin family. Unlike A4- and B2-crystallins (that were significantly increased withouttruncation), A- and B-crystallins were only truncated in EAU vitreous body. Taken as a whole, in therat EAU model, we suggest that post-translational truncations of A- and B-crystallins, phosphorylationof B-crystallin, and new production of A4- and B2-crystallins are intercorrelated with uveitisprogression and inflammatory responses.