Linoleic acid induces mouse embryonic stem cell proliferation via Ca2+/PKC, PI3K/Akt, and MAPKs

Cell Physiol Biochem. 2009;23(1-3):53-64. doi: 10.1159/000204090. Epub 2009 Feb 18.

Abstract

Aims: This study investigated the effect of linoleic acid (LA) on cell proliferation and the related signaling cascade in mouse embryonic stem (ES) cells.

Materials & methods: To examine effects of LA, mouse ES cells (ES-E14TG2a) were used. Moreover, DNA synthesis, glucose production, protein and mRNA expressions were measured.

Results: LA increased DNA synthesis in a concentration- (> or = 10(-9) M) and time- (> or = 24 h) dependent manner, as determined by [3H] thymidine incorporation and increased cell number. LA increased intracellular Ca2+ levels via regulation of phospholipase C (PLC) and activated protein kinase C (PKC). LA activated phosphatidylinositol 3-kinase (PI3K)/Akt and p44/42 mitogen-activated protein kinases (MAPKs). U73122 (PLC inhibitor), staurosporine (PKC inhibitor), LY294002 (PI3K inhibitor), and Akt inhibitor blocked the phosphorylation of p44/42 MAPKs. In addition, LA stimulated gluconeogenesis through increase expression of glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK). LA-induced increases in the cell cycle regulatory proteins, cyclin D1, cyclin E, cyclin-dependent kinase (CDK) 2, and CDK 4, were blocked by U73122, staurosporine, LY294002, Akt inhibitor, PD98059, and metformin (gluconeogenesis inhibitor).

Conclusion: LA stimulated cell proliferation via Ca2+, PLC/PKC, PI3K/Akt, and p44/42 MAPKs signaling pathways in mouse ES cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Western
  • Calcium / metabolism*
  • Cell Line
  • Cell Proliferation / drug effects
  • Embryonic Stem Cells / cytology
  • Embryonic Stem Cells / drug effects*
  • Flow Cytometry
  • Glucose / metabolism
  • Linoleic Acid / pharmacology*
  • Mice
  • Mitogen-Activated Protein Kinases / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Protein Kinase C / metabolism*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction / drug effects
  • Signal Transduction / physiology

Substances

  • Linoleic Acid
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • Protein Kinase C
  • Mitogen-Activated Protein Kinases
  • Glucose
  • Calcium