Marked increase of HGF mRNA in non-parenchymal liver cells of rats treated with hepatotoxins

Taisei Kinoshita, Kosuke Tashiro, Toshikazu Nakamura

研究成果: ジャーナルへの寄稿記事

248 引用 (Scopus)

抄録

When experimental hepatitis was induced by administrating rats with hepatotoxins such as CCl4 and D-galactosamine, HGF mRNA increased dramatically in the injured liver. The increase of HGF mRNA was time- and dose-dependent. At 5 hr after CCl4-treatment, HGF mRNA was remarkably increased; it reached the maximum level at 10 hr and maintained at this level for 40 hr. On the contrary, in D-galactosamine-induced hepatitis, HGF mRNA started to increase from 24 hr after a long lag time. Moreover, HGF mRNA was expressed transiently, decreasing rapidly to the basal level after reaching the maximum level at 36 hr. The degree of induction of HGF mRNA correlates well to the degree of liver damage. In the liver, HGF mRNA could be detected in only non-parenchymal cells, not in parenchymal hepatocytes. These findings suggest that liver is a main producing organ of HGF for liver regeneration after hepatic injury, and HGF is synthesized and secreted by non-parenchymal liver cells so that it stimulates the growth of parenchymal hepatocytes to repair liver tissue in paracrine fashion.

元の言語英語
ページ(範囲)1229-1234
ページ数6
ジャーナルBiochemical and Biophysical Research Communications
165
発行部数3
DOI
出版物ステータス出版済み - 12 30 1989

Fingerprint

Liver
Rats
Cells
Messenger RNA
Galactosamine
Hepatitis
Hepatocytes
Liver Regeneration
Repair
Tissue
Wounds and Injuries
Growth

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

これを引用

Marked increase of HGF mRNA in non-parenchymal liver cells of rats treated with hepatotoxins. / Kinoshita, Taisei; Tashiro, Kosuke; Nakamura, Toshikazu.

:: Biochemical and Biophysical Research Communications, 巻 165, 番号 3, 30.12.1989, p. 1229-1234.

研究成果: ジャーナルへの寄稿記事

@article{d71c23aff3d94eb7ae6bd79c527fe5ac,
title = "Marked increase of HGF mRNA in non-parenchymal liver cells of rats treated with hepatotoxins",
abstract = "When experimental hepatitis was induced by administrating rats with hepatotoxins such as CCl4 and D-galactosamine, HGF mRNA increased dramatically in the injured liver. The increase of HGF mRNA was time- and dose-dependent. At 5 hr after CCl4-treatment, HGF mRNA was remarkably increased; it reached the maximum level at 10 hr and maintained at this level for 40 hr. On the contrary, in D-galactosamine-induced hepatitis, HGF mRNA started to increase from 24 hr after a long lag time. Moreover, HGF mRNA was expressed transiently, decreasing rapidly to the basal level after reaching the maximum level at 36 hr. The degree of induction of HGF mRNA correlates well to the degree of liver damage. In the liver, HGF mRNA could be detected in only non-parenchymal cells, not in parenchymal hepatocytes. These findings suggest that liver is a main producing organ of HGF for liver regeneration after hepatic injury, and HGF is synthesized and secreted by non-parenchymal liver cells so that it stimulates the growth of parenchymal hepatocytes to repair liver tissue in paracrine fashion.",
author = "Taisei Kinoshita and Kosuke Tashiro and Toshikazu Nakamura",
year = "1989",
month = "12",
day = "30",
doi = "10.1016/0006-291X(89)92733-2",
language = "English",
volume = "165",
pages = "1229--1234",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "3",

}

TY - JOUR

T1 - Marked increase of HGF mRNA in non-parenchymal liver cells of rats treated with hepatotoxins

AU - Kinoshita, Taisei

AU - Tashiro, Kosuke

AU - Nakamura, Toshikazu

PY - 1989/12/30

Y1 - 1989/12/30

N2 - When experimental hepatitis was induced by administrating rats with hepatotoxins such as CCl4 and D-galactosamine, HGF mRNA increased dramatically in the injured liver. The increase of HGF mRNA was time- and dose-dependent. At 5 hr after CCl4-treatment, HGF mRNA was remarkably increased; it reached the maximum level at 10 hr and maintained at this level for 40 hr. On the contrary, in D-galactosamine-induced hepatitis, HGF mRNA started to increase from 24 hr after a long lag time. Moreover, HGF mRNA was expressed transiently, decreasing rapidly to the basal level after reaching the maximum level at 36 hr. The degree of induction of HGF mRNA correlates well to the degree of liver damage. In the liver, HGF mRNA could be detected in only non-parenchymal cells, not in parenchymal hepatocytes. These findings suggest that liver is a main producing organ of HGF for liver regeneration after hepatic injury, and HGF is synthesized and secreted by non-parenchymal liver cells so that it stimulates the growth of parenchymal hepatocytes to repair liver tissue in paracrine fashion.

AB - When experimental hepatitis was induced by administrating rats with hepatotoxins such as CCl4 and D-galactosamine, HGF mRNA increased dramatically in the injured liver. The increase of HGF mRNA was time- and dose-dependent. At 5 hr after CCl4-treatment, HGF mRNA was remarkably increased; it reached the maximum level at 10 hr and maintained at this level for 40 hr. On the contrary, in D-galactosamine-induced hepatitis, HGF mRNA started to increase from 24 hr after a long lag time. Moreover, HGF mRNA was expressed transiently, decreasing rapidly to the basal level after reaching the maximum level at 36 hr. The degree of induction of HGF mRNA correlates well to the degree of liver damage. In the liver, HGF mRNA could be detected in only non-parenchymal cells, not in parenchymal hepatocytes. These findings suggest that liver is a main producing organ of HGF for liver regeneration after hepatic injury, and HGF is synthesized and secreted by non-parenchymal liver cells so that it stimulates the growth of parenchymal hepatocytes to repair liver tissue in paracrine fashion.

UR - http://www.scopus.com/inward/record.url?scp=0024788217&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024788217&partnerID=8YFLogxK

U2 - 10.1016/0006-291X(89)92733-2

DO - 10.1016/0006-291X(89)92733-2

M3 - Article

C2 - 2692563

AN - SCOPUS:0024788217

VL - 165

SP - 1229

EP - 1234

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 3

ER -