DIFFERENTIAL EXPRESSION OF CYSTEINE-RICH INTESTINAL PROTEIN IN LIVER AND INTESTINE IN CCL4-INDUCED INFLAMMATION

Cysteine-rich intestinal protein (CRIP) is a double zinc finger (LIM d omain) protein that is developmentally regulated but has an unknown fu nction. CRIP is highly expressed in the intestine, but expression is l ow in liver. To determine if CRIP expression is regulated under altere d physiological status, we used CCl4-induced injury as a model to prod uce hepatic injury and systemic effects associated with inflammation. Since CRIP is a zinc finger protein and zinc decreases the hepatic res ponse 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 alanin e aminotransferase), indicating zinc did not have a protective effect. Liver CRIP mRNA increased with CCl4 and CRIP protein was shown by imm unohistochemistry to be localized in hepatocytes near the vascular sup ply. 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 cell ular damage due to acute hepatic injury and are consistent with a func tional role for CRIP in proliferation, differentiation, or turnover.