Leptin Induces Mitogen-activated Protein Kinase- dependent Proliferation of C3H10T1/2 Cells

Leptin, secreted by adipocytes, regulates satiety and energy expenditure. Several forms of leptin receptors produced by alternative mRNA splicing are found in many tissues, including the hypothalamus, liver, lung, kidney, hematopoietic cells, and gonads, suggesting that leptin exerts effects in thes...

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Published inThe Journal of biological chemistry Vol. 272; no. 20; pp. 12897 - 12900
Main Authors Takahashi, Yutaka, Okimura, Yasuhiko, Mizuno, Ishikazu, Iida, Keiji, Takahashi, Tetsuya, Kaji, Hidesuke, Abe, Hiromi, Chihara, Kazuo
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 16.05.1997
American Society for Biochemistry and Molecular Biology
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Abstract Leptin, secreted by adipocytes, regulates satiety and energy expenditure. Several forms of leptin receptors produced by alternative mRNA splicing are found in many tissues, including the hypothalamus, liver, lung, kidney, hematopoietic cells, and gonads, suggesting that leptin exerts effects in these tissues. In accordance with the distribution of leptin receptors, there is accumulating evidence that leptin plays various roles in reproduction, hematopoiesis, and the immune systems in addition to the regulation of food intake and energy expenditure. In the present study, we examined the in vitro effects of leptin on proliferation of a mouse embryonic cell line, C3H10T1/2, and its mechanism of action. Leptin caused a dose- and time-dependent increase in mitogen-activated protein kinase (MAPK) activity that was accompanied by an increase in C3H10T1/2 cell number. The MAPK kinase-1-specific inhibitor PD98059 completely blocked the increases in both MAPK activity and cell proliferation caused by leptin. These findings indicate that leptin stimulates the proliferation of C3H10T1/2 cells via the MAPK cascade.
AbstractList Leptin, secreted by adipocytes, regulates satiety and energy expenditure. Several forms of leptin receptors produced by alternative mRNA splicing are found in many tissues, including the hypothalamus, liver, lung, kidney, hematopoietic cells, and gonads, suggesting that leptin exerts effects in these tissues. In accordance with the distribution of leptin receptors, there is accumulating evidence that leptin plays various roles in reproduction, hematopoiesis, and the immune systems in addition to the regulation of food intake and energy expenditure. In the present study, we examined the in vitro effects of leptin on proliferation of a mouse embryonic cell line, C3H10T1/2, and its mechanism of action. Leptin caused a dose- and time-dependent increase in mitogen-activated protein kinase (MAPK) activity that was accompanied by an increase in C3H10T1/2 cell number. The MAPK kinase-1-specific inhibitor PD98059 completely blocked the increases in both MAPK activity and cell proliferation caused by leptin. These findings indicate that leptin stimulates the proliferation of C3H10T1/2 cells via the MAPK cascade.
Leptin, secreted by adipocytes, regulates satiety and energy expenditure. Several forms of leptin receptors produced by alternative mRNA splicing are found in many tissues, including the hypothalamus, liver, lung, kidney, hematopoietic cells, and gonads, suggesting that leptin exerts effects in these tissues. In accordance with the distribution of leptin receptors, there is accumulating evidence that leptin plays various roles in reproduction, hematopoiesis, and the immune systems in addition to the regulation of food intake and energy expenditure. In the present study, we examined the in vitro effects of leptin on proliferation of a mouse embryonic cell line, C3H10T1/2, and its mechanism of action. Leptin caused a dose- and time-dependent increase in mitogen-activated protein kinase (MAPK) activity that was accompanied by an increase in C3H10T1/2 cell number. The MAPK kinase-1-specific inhibitor PD98059 completely blocked the increases in both MAPK activity and cell proliferation caused by leptin. These findings indicate that leptin stimulates the proliferation of C3H10T1/2 cells via the MAPK cascade.
Author Okimura, Yasuhiko
Takahashi, Tetsuya
Abe, Hiromi
Kaji, Hidesuke
Chihara, Kazuo
Mizuno, Ishikazu
Takahashi, Yutaka
Iida, Keiji
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  givenname: Ishikazu
  surname: Mizuno
  fullname: Mizuno, Ishikazu
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  givenname: Keiji
  surname: Iida
  fullname: Iida, Keiji
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  givenname: Tetsuya
  surname: Takahashi
  fullname: Takahashi, Tetsuya
– sequence: 6
  givenname: Hidesuke
  surname: Kaji
  fullname: Kaji, Hidesuke
– sequence: 7
  givenname: Hiromi
  surname: Abe
  fullname: Abe, Hiromi
– sequence: 8
  givenname: Kazuo
  surname: Chihara
  fullname: Chihara, Kazuo
BackLink https://www.ncbi.nlm.nih.gov/pubmed/9148892$$D View this record in MEDLINE/PubMed
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Snippet Leptin, secreted by adipocytes, regulates satiety and energy expenditure. Several forms of leptin receptors produced by alternative mRNA splicing are found in...
Leptin, secreted by adipocytes, regulates satiety and energy expenditure. Several forms of leptin receptors produced by alternative mRNA splicing are found in...
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SubjectTerms Animals
Calcium-Calmodulin-Dependent Protein Kinases - metabolism
Cell Division - drug effects
Cell Line
Dose-Response Relationship, Drug
Enzyme Inhibitors - pharmacology
Female
Flavonoids - pharmacology
Leptin
Mice
Pregnancy
Proteins - pharmacology
Signal Transduction - drug effects
Title Leptin Induces Mitogen-activated Protein Kinase- dependent Proliferation of C3H10T1/2 Cells
URI https://dx.doi.org/10.1074/jbc.272.20.12897
http://www.jbc.org/content/272/20/12897.abstract
https://www.ncbi.nlm.nih.gov/pubmed/9148892
Volume 272
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