Proinsulin C-peptide induces c-Jun N-terminal kinase 1 expression in LEII mouse lung capillary endothelial cells

Jpn J Vet Res. 2009 Nov;57(3):163-7.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • C-Peptide / pharmacology*
  • Cell Line
  • Endothelial Cells / metabolism*
  • Enzyme Inhibitors / pharmacology
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Flavonoids / pharmacology
  • Gene Expression Regulation, Enzymologic
  • Lung / blood supply*
  • Mice
  • Mitogen-Activated Protein Kinase 8 / metabolism*
  • RNA, Messenger / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • C-Peptide
  • Enzyme Inhibitors
  • Flavonoids
  • RNA, Messenger
  • Extracellular Signal-Regulated MAP Kinases
  • Mitogen-Activated Protein Kinase 8
  • p38 Mitogen-Activated Protein Kinases
  • 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one