COEXPRESSION OF PERIPORTAL AND PERIVENOUS ENZYMES IN RAT HEPATOCYTES AFTER EXPERIMENTAL BILE-DUCT LIGATION - COMPARISON WITH INTRASPLENICALLY TRANSPLANTED HEPATOCYTES

Citation
L. Racinesamson et al., COEXPRESSION OF PERIPORTAL AND PERIVENOUS ENZYMES IN RAT HEPATOCYTES AFTER EXPERIMENTAL BILE-DUCT LIGATION - COMPARISON WITH INTRASPLENICALLY TRANSPLANTED HEPATOCYTES, HISTOCHEM C, 105(4), 1996, pp. 319-329
Citations number
30
Categorie Soggetti
Cell Biology",Microscopy
Journal title
HISTOCHEMISTRY AND CELL BIOLOGY
ISSN journal
09486143 → ACNP
Volume
105
Issue
4
Year of publication
1996
Pages
319 - 329
Database
ISI
SICI code
0948-6143(1996)105:4<319:COPAPE>2.0.ZU;2-#
Abstract
The coexpression of normally periportal and perivenous markers has bee n described in heterotopically transplanted hepatocytes. To determine whether such a coexpression might also occur in hepatocytes retaining their original intrahepatic location, we compared in bile-duct-ligated livers and intrasplenically transplanted hepatocytes, the expression and distribution of the predominantly periportal glucose-6-phosphatase , succinate dehydrogenase, and lactate dehydrogenase, the predominantl y perivenous glutamate dehydrogenase, NADPH-dehydrogenase, and beta-hy droxybutyrate dehydrogenase, and the strictly perivenous glutamine syn thetase. The coexpression of high levels of the two periportal markers glucose-6-phosphatase and lactate dehydrogenase and of the perivenous marker NADPH dehydrogenase was observed in two situations: in cluster s of hepatocytes isolated within the ductular proliferation in bile-du ct-ligated livers and the majority of intrasplenically transplanted he patocytes. The expression of glutamine synthetase was different accord ing to the site. The protein was observed in certain intrasplenically transplanted hepatocytes bordering the splenic vessels but was never d etected in hepatocyte clusters found in bile-duct-ligated livers. Our study therefore suggests that the coexpression of periportal and periv enous markers in the same hepatocytes is likely to be a non-specific c onsequence of the loss of the normal connections of hepatocytes with t he normal liver microcirculation.