Hepatic expression of metallothionein I/II, glycoprotein 96, IL-6, and TGF- β in rat strains with different susceptibilities to experimental autoimmune encephalomyelitis.

Hepatic expression of metallothionein I/II, glycoprotein 96, IL-6, and TGF- β in rat strains with different susceptibilities to experimental autoimmune encephalomyelitis.
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DOI:
10.1155/2013/750406
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发表时间:
2013
影响因子:
--
通讯作者:
Radošević-Stašić B
Radošević-Stašić B
中科院分区:
其他
文献类型:
--
作者:
Grubić-Kezele T;Blagojević Zagorac G;Jakovac H;Domitrović R;Milin C;Radošević-Stašić B

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在寻找可能导致 Albino Oxford (AO) 和 Dark Agouti (DA) 大鼠对 EAE 易感性差异的外周因素时,我们估计了这些动物肝脏中金属硫蛋白 I/II (MT)、热休克蛋白 -gp96、白细胞介素 (IL)-6 和转化生长因子 (TGF)-β 的表达。用完全弗氏佐剂(CFA)中乳化的牛脑匀浆(BBH)或仅用CFA对大鼠进行免疫。免疫印迹和免疫组织化学分析在免疫后第 12 天以及在完整大鼠中进行。数据显示,在 EAE 第一次发作期间,只有易患 EAE 的 DA 大鼠的肝脏 MT、gp96、IL-6 和 TGF-β 显着上调。相反,AO大鼠在完整肝脏中MT I/II、IL-6和TGF-β的表达显着较高(P < 0,001),表明这些蛋白的较高组成型表达有助于EAE的抵抗。此外,由于之前我们发现 AO 大鼠对免疫反应的反应是通过几种肝结构(血管内皮、库普弗细胞和肝细胞)上 TGF-β 的早期上调,因此数据表明,特定的肝脏微环境也可能有助于这些大鼠从 EAE 中更快恢复。
In a search of peripheral factors that could be responsible for the discrepancy in susceptibility to EAE in Albino Oxford (AO) and Dark Agouti (DA) rats, we estimated the expression of metallothioneins I/II (MT), heat shock protein-gp96, interleukin (IL)-6, and transforming growth factor (TGF)-β in the livers of these animals. Rats were immunized with bovine brain homogenate (BBH) emulsified in complete Freund adjuvant (CFA) or only with CFA. Western blot and immunohistochemical analyses were done on day 12 after the immunization, as well as in intact rats. The data have shown that during the first attack of EAE only the EAE prone-DA rats markedly upregulated the hepatic MTs, gp96, IL-6, and TGF-β. In contrast, AO rats had a significantly higher expression of MT I/II, IL-6, and TGF-β in intact liver (P < 0,001), suggesting that the greater constitutive expression of these proteins contributed to the resistance of EAE. Besides, since previously we found that AO rats reacted on immunization by an early upregulation of TGF-β on several hepatic structures (vascular endothelium, Kupffer cells, and hepatocytes), the data suggest that the specific hepatic microenvironment might contribute also to the faster recovery of these rats from EAE.
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