Increased heme oxygenase-1 gene expression in liver cells and splanchnic organs from portal hypertensive rats

Citation
M. Fernandez et Hl. Bonkovsky, Increased heme oxygenase-1 gene expression in liver cells and splanchnic organs from portal hypertensive rats, HEPATOLOGY, 29(6), 1999, pp. 1672-1679
Citations number
57
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
HEPATOLOGY
ISSN journal
02709139 → ACNP
Volume
29
Issue
6
Year of publication
1999
Pages
1672 - 1679
Database
ISI
SICI code
0270-9139(199906)29:6<1672:IHOGEI>2.0.ZU;2-Q
Abstract
Heme oxygenase (HO) catalyzes the conversion of heme into biliverdin, iron, and carbon monoxide (CO). Two isoforms of WO have been identified: the ind ucible HO-1 and the constitutive HO-2. CO, like nitric oxide, is an endogen ous vasodilator that could contribute to modulation of systemic and local v ascular tone. The aim of the present study was to determine the expression of HO isoforms in liver cells and splanchnic organs from portal hypertensiv e (PPI) and sham-operated (SO) rats. Liver cells (hepatocytes, Kupffer and stellate tells), and splanchnic organs (liver, mesentery, intestine, colon, and spleen) were isolated From PH and SO rats. Expression of HO mRNA and p rotein was assessed by reverse-transcription polymerase chain reaction (RT- PCR) and Western blot analysis, respectively. In SO rats, HO-1 mRNA express ion was only detected in spleen. In contrast, in PH rats, HO-1 mRNA was exp ressed in hepatocytes, Kupffer cells, and in all the splanchnic organs stud ied. Moreover, levels of HO-1 protein in splanchnic organs were significant ly higher in PH rats than in SO animals. In addition, HO-2 expression was o bserved in all liver cell types and splanchnic organs studied from both PH and SO rats. These results indicate that HO-2 is expressed in parenchymal a nd nonparenchymal liver cells, as well as splanchnic organs, of both PH and SO rats. In addition, HO-I is up-regulated in hepatocytes and splanchnic o rgans of PH rats, compared with SO animals, suggesting a possible pathophys iological role of HO-1 in chronic portal hypertension.