Expression of hepatic thrombopoietin mRNA in primary cultured hepatocytes and in rats with acute liver injury or bone marrow suppression with or without cirrhosis

Toru Ishikawa, Takafumi Ichida, Yasunobu Matsuda, Soichi Sugitani, Motoya Sugiyama, Takashi Kato, Hiroshi Miyazaki, Hitoshi Asakura

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Background and Aims: The main causes of thrombocytopenia in cirrhosis are thought to be platelet destruction and the reduction of thrombopoietin (TPO) expression in the liver. The mechanisms by which levels of TPO mRNA are regulated in cirrhosis have not been elucidated. In this study, we investigated some possible mechanisms. Methods: We used three experimental models: bone marrow suppression, acute liver injury and primary cultured hepatocytes. We used northern blots to assess the kinetics of TPO mRNA expression in the livers of irradiated rats (with and without cirrhosis) in acute liver injury and in primary cultured hepatocytes treated with hepatotoxin or cytokines. Results: Although the bone marrow was hypocellular, there was no apparent enhancement of TPO mRNA expression in the irradiated rats with cirrhotic livers compared with the unirradiated rats with cirrhotic livers. There were no conspicuous changes in hepatic TPO mRNA expression between the livers of the control rats and the three models of acute liver injury. There were no conspicuous changes in the levels of TPO mRNA between control hepatocytes and hepatocytes treated with hepatotoxin or cytokines. Conclusions: Our results suggest that bone marrow is not a regulator of hepatic TPO production in cirrhosis. The reduced TPO mRNA expression found in cirrhotic rats may not result merely from serious cellular damage; it may be associated with cirrhosis-specific regulatory mechanisms for the expression of the TPO gene. Further studies are needed to search for other factors that may induce reduced TPO expression. (C) 2000 Blackwell Science Asia Pty Ltd.

Original languageEnglish
Pages (from-to)647-653
Number of pages7
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume15
Issue number6
DOIs
Publication statusPublished - 2000
Externally publishedYes

Fingerprint

Thrombopoietin
Hepatocytes
Fibrosis
Bone Marrow
Messenger RNA
Liver
Wounds and Injuries
Cytokines
Thrombocytopenia
Northern Blotting
Theoretical Models
Blood Platelets

Keywords

  • Acute liver injury
  • Bone marrow suppression
  • Irradiation
  • Liver cirrhosis
  • Messenger RNA
  • Northern blotting
  • Rat liver
  • Thrombopoietin

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Cite this

Expression of hepatic thrombopoietin mRNA in primary cultured hepatocytes and in rats with acute liver injury or bone marrow suppression with or without cirrhosis. / Ishikawa, Toru; Ichida, Takafumi; Matsuda, Yasunobu; Sugitani, Soichi; Sugiyama, Motoya; Kato, Takashi; Miyazaki, Hiroshi; Asakura, Hitoshi.

In: Journal of Gastroenterology and Hepatology (Australia), Vol. 15, No. 6, 2000, p. 647-653.

Research output: Contribution to journalArticle

Ishikawa, Toru ; Ichida, Takafumi ; Matsuda, Yasunobu ; Sugitani, Soichi ; Sugiyama, Motoya ; Kato, Takashi ; Miyazaki, Hiroshi ; Asakura, Hitoshi. / Expression of hepatic thrombopoietin mRNA in primary cultured hepatocytes and in rats with acute liver injury or bone marrow suppression with or without cirrhosis. In: Journal of Gastroenterology and Hepatology (Australia). 2000 ; Vol. 15, No. 6. pp. 647-653.
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T1 - Expression of hepatic thrombopoietin mRNA in primary cultured hepatocytes and in rats with acute liver injury or bone marrow suppression with or without cirrhosis

AU - Ishikawa, Toru

AU - Ichida, Takafumi

AU - Matsuda, Yasunobu

AU - Sugitani, Soichi

AU - Sugiyama, Motoya

AU - Kato, Takashi

AU - Miyazaki, Hiroshi

AU - Asakura, Hitoshi

PY - 2000

Y1 - 2000

N2 - Background and Aims: The main causes of thrombocytopenia in cirrhosis are thought to be platelet destruction and the reduction of thrombopoietin (TPO) expression in the liver. The mechanisms by which levels of TPO mRNA are regulated in cirrhosis have not been elucidated. In this study, we investigated some possible mechanisms. Methods: We used three experimental models: bone marrow suppression, acute liver injury and primary cultured hepatocytes. We used northern blots to assess the kinetics of TPO mRNA expression in the livers of irradiated rats (with and without cirrhosis) in acute liver injury and in primary cultured hepatocytes treated with hepatotoxin or cytokines. Results: Although the bone marrow was hypocellular, there was no apparent enhancement of TPO mRNA expression in the irradiated rats with cirrhotic livers compared with the unirradiated rats with cirrhotic livers. There were no conspicuous changes in hepatic TPO mRNA expression between the livers of the control rats and the three models of acute liver injury. There were no conspicuous changes in the levels of TPO mRNA between control hepatocytes and hepatocytes treated with hepatotoxin or cytokines. Conclusions: Our results suggest that bone marrow is not a regulator of hepatic TPO production in cirrhosis. The reduced TPO mRNA expression found in cirrhotic rats may not result merely from serious cellular damage; it may be associated with cirrhosis-specific regulatory mechanisms for the expression of the TPO gene. Further studies are needed to search for other factors that may induce reduced TPO expression. (C) 2000 Blackwell Science Asia Pty Ltd.

AB - Background and Aims: The main causes of thrombocytopenia in cirrhosis are thought to be platelet destruction and the reduction of thrombopoietin (TPO) expression in the liver. The mechanisms by which levels of TPO mRNA are regulated in cirrhosis have not been elucidated. In this study, we investigated some possible mechanisms. Methods: We used three experimental models: bone marrow suppression, acute liver injury and primary cultured hepatocytes. We used northern blots to assess the kinetics of TPO mRNA expression in the livers of irradiated rats (with and without cirrhosis) in acute liver injury and in primary cultured hepatocytes treated with hepatotoxin or cytokines. Results: Although the bone marrow was hypocellular, there was no apparent enhancement of TPO mRNA expression in the irradiated rats with cirrhotic livers compared with the unirradiated rats with cirrhotic livers. There were no conspicuous changes in hepatic TPO mRNA expression between the livers of the control rats and the three models of acute liver injury. There were no conspicuous changes in the levels of TPO mRNA between control hepatocytes and hepatocytes treated with hepatotoxin or cytokines. Conclusions: Our results suggest that bone marrow is not a regulator of hepatic TPO production in cirrhosis. The reduced TPO mRNA expression found in cirrhotic rats may not result merely from serious cellular damage; it may be associated with cirrhosis-specific regulatory mechanisms for the expression of the TPO gene. Further studies are needed to search for other factors that may induce reduced TPO expression. (C) 2000 Blackwell Science Asia Pty Ltd.

KW - Acute liver injury

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