Biological and immunological properties of human hepatocyte growth factor from plasma of patients with fulminant hepatic failure

Gohda, Eiichi; Yamasaki, Toshiko; Tsubouchi, Hirohito; Kurobe, Masayuki; Sakiyama, Osamu; Aoki, Hisakazu; Niidani, Nobuyuki; Shin, Sadahito; Hayashi, Kyozo; Hashimoto, Shuji; Daikuhara, Yasushi; Yamamoto, Ichiro

doi:10.1016/0167-4889(90)90020-e

Cited by 47 publications

(19 citation statements)

References 30 publications

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“…These growth factors are induced during liver regeneration in vivo, such as liver injury and partial hepatectomy, and an additive effect of TGF-␣ and HGF on DNA synthesis in primary cultured hepatocytes has been reported (23,24). In response to growth factors, Ras/MAPK, phosphatidyl inositol-3 kinase (PI3K) (25) and Janus kinase (Jak)/signal transducer and activator of transcription (STAT) (26) are activated in hepatocytes.…”

Section: Discussionmentioning

confidence: 98%

Additive and Inhibitory Effects of Simultaneous Treatment with Growth Factors on DNA Synthesis through MAPK Pathway and G1 Cyclins in Rat Hepatocytes

Moriuchi

Hirono

Ido

et al. 2001

Biochemical and Biophysical Research Communications

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Section: Discussionmentioning

confidence: 98%

Additive and Inhibitory Effects of Simultaneous Treatment with Growth Factors on DNA Synthesis through MAPK Pathway and G1 Cyclins in Rat Hepatocytes

Moriuchi

Hirono

Ido

et al. 2001

Biochemical and Biophysical Research Communications

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“…IGF-1 cannot stimulate DNA synthesis or proliferation of hepatocytes in vitro [10], and there are few IGF-1 receptors present on hypatocytes [11]. Despite this, liver growth in GH-deficient animals exposed to IGF-1 is in proportion to body growth but less pronounced than that of high doses of GH [9].…”

Section: Discussionmentioning

confidence: 99%

“…For instance, such an effect could be mediated by increased metabolic demands. During normal conditions, hepatocytes have very few IGF-1 receptors and they do not proliferate in vitro in response to IGF-1 [10][11][12]. This argues against autocrine effects of hepatocyte-produced IGF.…”

Section: Introductionmentioning

confidence: 96%

Possible Roles of Insulin-Like Growth Factor in Regulation of Physiological and Pathophysiological Liver Growth

Skrtic¹,

Wallenius²,

Sjögren³

et al. 2001

Horm Res Paediatr

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Background/Aims: Almost all circulating insulin-like growth factor-1 (IGF-1) is produced and secreted from the liver. However, the possible role of IGF-1 in local regulation of liver functions including liver growth is unclear. In the present study, we investigated the role of IGF-1 on liver growth in vivo and in hepatic stellate cell function in vitro. Results: Liver-specific knock-out of the IGF-1 gene by use of the cre-loxP system caused enhanced liver growth, possibly reflecting increased growth hormone (GH) secretion due to decreased negative feedback by IGF-1. Studies on cultured rat hepatic stellate cells (HSC) showed that IGF-1 and hepatocyte-conditioned medium (PCcM) time- and dose-dependently increased hepatocyte growth factor (HGF) mRNA and HGF immunoreactivity. IGF-1 and PCcM also enhanced DNA synthesis in the HSC cultures. The PCcM did not contain bioactive IGF-1 and was also able to stimulate proliferation when prepared under serum- and hormone-free conditions. Conclusion: In vivo results show that IGF-1 is not essential for normal growth of the intact liver. The in vitro results indicate that both IGF-1 and IGF- 1-independent factor(s) from hepatocytes can stimulate HGF production by HSC. It remains to be investigated whether these effects are of importance for liver regeneration or pathological conditions.

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“…IGF-I production by the liver is achieved very early during postnatal life as a function of the hormonal status of the rat [10,11]. Although IGF-I was originally identified based on its ability to stimulate proliferation of various cell types in vitro [6], hepatocytes in vitro do not proliferate in response to IGF-I [12]. Moreover, hepatocytes of the normal liver have few IGF-I receptors [13], arguing against autocrine effects of hepatocyte-produced IGF.…”

Section: Introductionmentioning

confidence: 98%

Suppression of transforming growth factor-β results in upregulation of transcription of regeneration factors after chronic liver injury

Nakamura

Ueno

Sakamoto

et al. 2004

Journal of Hepatology

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Biological and immunological properties of human hepatocyte growth factor from plasma of patients with fulminant hepatic failure

Cited by 47 publications

References 30 publications

Additive and Inhibitory Effects of Simultaneous Treatment with Growth Factors on DNA Synthesis through MAPK Pathway and G1 Cyclins in Rat Hepatocytes

Additive and Inhibitory Effects of Simultaneous Treatment with Growth Factors on DNA Synthesis through MAPK Pathway and G1 Cyclins in Rat Hepatocytes

Possible Roles of Insulin-Like Growth Factor in Regulation of Physiological and Pathophysiological Liver Growth

Suppression of transforming growth factor-β results in upregulation of transcription of regeneration factors after chronic liver injury

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