Khoo C, Hallquist N A, Samuelson D A, Cousins R J
Food Science and Human Nutrition Department, University of Florida, Gainesville 32611, USA.
Am J Physiol. 1996 Apr;270(4 Pt 1):G613-8. doi: 10.1152/ajpgi.1996.270.4.G613.
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.
富含半胱氨酸的肠道蛋白（CRIP）是一种双锌指（LIM结构域）蛋白，其表达受发育调控，但功能未知。CRIP在肠道中高度表达，而在肝脏中表达较低。为了确定CRIP表达在生理状态改变时是否受到调控，我们以四氯化碳诱导的损伤为模型，引发肝损伤及与炎症相关的全身效应。由于CRIP是一种锌指蛋白，且锌可降低肝脏对四氯化碳的反应，因此我们还研究了补充膳食锌（300毫克/千克饮食）的效果。我们的结果表明，这种膳食锌补充水平并未影响肝损伤指标（血浆丙氨酸转氨酶），表明锌没有保护作用。肝脏CRIP mRNA随四氯化碳而增加，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，四氯化碳导致CRIP mRNA短暂下降，但补充膳食锌处理可防止这种下降。这些当前结果表明，CRIP表达会因急性肝损伤导致的细胞损伤而发生变化，这与CRIP在增殖、分化或更新中的功能作用一致。
