Differential expression of cysteine-rich intestinal protein in liver and intestine in CCl4-induced inflammation.
Differential expression of cysteine-rich intestinal protein in liver and intestine in CCl4-induced inflammation.
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CCl4 诱导的炎症中肝脏和肠道中富含半胱氨酸的肠蛋白的差异表达。
DOI：
10.1152/ajpgi.1996.270.4.g613
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Cousins,RJ
中科院分区：
文献类型：
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作者：
Khoo,C;Hallquist,NA;Samuelson,DA;Cousins,RJ
富含半胱氨酸的肠蛋白（CRIP）是一种双锌指（LIM结构域）蛋白，其受发育调控，但功能未知。CRIP在肠中高度表达，但在肝脏中表达较低。为了确定CRIP表达是否在改变的生理状态下受到调节，我们使用CCl 4诱导的损伤作为模型来产生与炎症相关的肝损伤和全身效应。由于CRIP是一种锌指蛋白，锌可降低肝脏对CCl 4的反应，因此还检查了补充膳食锌（300 mg/kg膳食）的作用。我们的研究结果表明，这一水平的饲料锌没有影响肝损伤指数（血浆丙氨酸氨基转移酶），表明锌没有保护作用。肝CRIP mRNA随着CCl 4的增加而增加，免疫组织化学显示CRIP蛋白定位于血管供应附近的肝细胞中。在肠道中，CCl 4引起CRIP mRNA的短暂减少，但补充膳食锌治疗阻止了这种减少。这些目前的结果表明，CRIP表达的变化响应于细胞损伤，由于急性肝损伤，并与CRIP在增殖，分化，或营业额的功能作用是一致的。
Cysteine-rich intestinal protein (CRIP) is a double zinc finger (LIM domain) protein that is developmentally regulated but has an unknown function. CRIP is highly expressed in the intestine, but expression is low in liver. To determine if CRIP expression is regulated under altered physiological status, we used CCl4-induced injury as a model to produce hepatic injury and systemic effects associated with inflammation. Since CRIP is a zinc finger protein and zinc decreases the hepatic response to CCl4, the effect of supplemental dietary zinc (300 mg/kg diet) was also examined. Our results show that this supplemental level of dietary zinc did not affect the index of hepatic injury (plasma alanine aminotransferase), indicating zinc did not have a protective effect. Liver CRIP mRNA increased with CCl4 and CRIP protein was shown by immunohistochemistry to be localized in hepatocytes near the vascular supply. In the intestine, CCl4 caused a transient decrease in CRIP mRNA, but supplemental dietary zinc treatment prevented this decrease. These current results show that CRIP expression changes in response to cellular damage due to acute hepatic injury and are consistent with a functional role for CRIP in proliferation, differentiation, or turnover.