Abstract
To characterize the roles of C-peptide in vascular homeostatic processes, we examined the genes regulated by C-peptide in LEII mouse lung microvascular endothelial cells. Treatment of the cells with C-peptide increased the expression of c-Jun N-terminal kinase 1 (JNK1) mRNA dose-dependently, accompanied by an increase in JNK1 protein content. Prior treatment of the cells with PD98059, an ERK kinase inhibitor or SB203580, a p38MAPK inhibitor, abrogated the C-peptide-elicited JNK1 mRNA expression. These results indicate that C-peptide increases JNK1 protein levels, possibly through ERK- and p38MAPK-dependent activation of JNK gene transcription.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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C-Peptide / pharmacology*
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Cell Line
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Endothelial Cells / metabolism*
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Enzyme Inhibitors / pharmacology
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Extracellular Signal-Regulated MAP Kinases / metabolism
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Flavonoids / pharmacology
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Gene Expression Regulation, Enzymologic
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Lung / blood supply*
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Mice
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Mitogen-Activated Protein Kinase 8 / metabolism*
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RNA, Messenger / metabolism
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p38 Mitogen-Activated Protein Kinases / metabolism
Substances
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C-Peptide
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Enzyme Inhibitors
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Flavonoids
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RNA, Messenger
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Extracellular Signal-Regulated MAP Kinases
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Mitogen-Activated Protein Kinase 8
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p38 Mitogen-Activated Protein Kinases
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2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one