Increased heme oxygenase-1 gene expression in the livers of patients with portal hypertension due to severe hepatic cirrhosis

M. Matsumi, T. Takahashi, H. Fujii, I. Ohashi, Ryuji Kaku, H. Nakatsuka, H. Shimizu, K. Morita, M. Hirakawa, M. Inagaki, H. Sadamori, Takahito Yagi, N. Tanaka, R. Akagi

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Surgical bleeding associated with splanchnic hyperaemia due to portal hypertension complicates the anaesthetic management of hepatic transplantation. Although the mechanism(s) of portal hypertension are not fully understood, carbon monoxide, a product of the heme oxygenase (HO) reaction, is thought to be one of the endogenous vasodilators in the liver. In this study, the expression of mRNA encoding inducible HO isozyme (HO-1) in the livers of patients with portal hypertension undergoing hepatic transplantation was determined in comparison with those without portal hypertension. HO-1 mRNA levels were significantly greater in the portal hypertension group than in the group without portal hypertension. In contrast with HO-1, the gene expression of non-specific δ-amino-levulinate synthase (ALAS-N), which is down-regulated by heme in the liver, was the same in both groups. These results suggest that HO-1 is up-regulated through heme-independent stimuli according to the development of portal hypertension, and that induced HO-1 plays a pathophysiological role in portal hypertension through carbon monoxide production.

Original languageEnglish
Pages (from-to)282-288
Number of pages7
JournalJournal of International Medical Research
Volume30
Issue number3
Publication statusPublished - 2002

Fingerprint

Heme Oxygenase-1
Portal Hypertension
Gene expression
Liver Cirrhosis
Liver
Gene Expression
Heme Oxygenase (Decyclizing)
Carbon Monoxide
Heme
Liver Transplantation
Messenger RNA
Viscera
Hyperemia
Vasodilator Agents
Isoenzymes
Anesthetics
Hemorrhage

Keywords

  • Gene expression
  • Heme oxygenase-1
  • Hepatic transplantation
  • Liver cirrhosis
  • Non-specific δ-aminolevulinate synthase
  • Portal hypertension

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Increased heme oxygenase-1 gene expression in the livers of patients with portal hypertension due to severe hepatic cirrhosis. / Matsumi, M.; Takahashi, T.; Fujii, H.; Ohashi, I.; Kaku, Ryuji; Nakatsuka, H.; Shimizu, H.; Morita, K.; Hirakawa, M.; Inagaki, M.; Sadamori, H.; Yagi, Takahito; Tanaka, N.; Akagi, R.

In: Journal of International Medical Research, Vol. 30, No. 3, 2002, p. 282-288.

Research output: Contribution to journalArticle

Matsumi, M, Takahashi, T, Fujii, H, Ohashi, I, Kaku, R, Nakatsuka, H, Shimizu, H, Morita, K, Hirakawa, M, Inagaki, M, Sadamori, H, Yagi, T, Tanaka, N & Akagi, R 2002, 'Increased heme oxygenase-1 gene expression in the livers of patients with portal hypertension due to severe hepatic cirrhosis', Journal of International Medical Research, vol. 30, no. 3, pp. 282-288.
Matsumi, M. ; Takahashi, T. ; Fujii, H. ; Ohashi, I. ; Kaku, Ryuji ; Nakatsuka, H. ; Shimizu, H. ; Morita, K. ; Hirakawa, M. ; Inagaki, M. ; Sadamori, H. ; Yagi, Takahito ; Tanaka, N. ; Akagi, R. / Increased heme oxygenase-1 gene expression in the livers of patients with portal hypertension due to severe hepatic cirrhosis. In: Journal of International Medical Research. 2002 ; Vol. 30, No. 3. pp. 282-288.
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AB - Surgical bleeding associated with splanchnic hyperaemia due to portal hypertension complicates the anaesthetic management of hepatic transplantation. Although the mechanism(s) of portal hypertension are not fully understood, carbon monoxide, a product of the heme oxygenase (HO) reaction, is thought to be one of the endogenous vasodilators in the liver. In this study, the expression of mRNA encoding inducible HO isozyme (HO-1) in the livers of patients with portal hypertension undergoing hepatic transplantation was determined in comparison with those without portal hypertension. HO-1 mRNA levels were significantly greater in the portal hypertension group than in the group without portal hypertension. In contrast with HO-1, the gene expression of non-specific δ-amino-levulinate synthase (ALAS-N), which is down-regulated by heme in the liver, was the same in both groups. These results suggest that HO-1 is up-regulated through heme-independent stimuli according to the development of portal hypertension, and that induced HO-1 plays a pathophysiological role in portal hypertension through carbon monoxide production.

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