Differential expression of cysteine-rich intestinal protein in
liver and intestine in carbon tetrachloride-induced inflammation.
Khoo, C., N. A. Hallquist, D. A. Samuelson, and R. J. Cousins.
Food Science and Human Nutrition Department, Center for Nutritional
Sciences and Small Animal Clinical Sciences, University of Florida,
Gainesville, FL 32611
APStracts 2:0194G, 1995.
Cysteine-rich intestinal protein (CRIP) is a double zinc finger (LIM
domain) protein which 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 physiologic 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 the response to cellular damage due to
acute hepatic injury and are consistent with a functional role for
CRIP in proliferation, differentiation or turnover.
Received 13 June 1995; accepted in final form 30 September 1995.
APS Manuscript Number G250-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95