Induction of cysteine-rich motor neuron 1 mRNA expression in vascular endothelial cells

Biochem Biophys Res Commun. 2014 Aug 22;451(2):235-8. doi: 10.1016/j.bbrc.2014.07.108. Epub 2014 Jul 30.

Abstract

Cysteine-rich motor neuron 1 (CRIM1) is expressed in vascular endothelial cells and plays a crucial role in angiogenesis. In this study, we investigated the expression of CRIM1 mRNA in human umbilical vein endothelial cells (HUVECs). CRIM1 mRNA levels were not altered in vascular endothelial growth factor (VEGF)-stimulated monolayer HUVECs or in cells in collagen gels without VEGF. In contrast, the expression of CRIM1 mRNA was elevated in VEGF-stimulated cells in collagen gels. The increase in CRIM1 mRNA expression was observed even at 2h when HUVECs did not form tubular structures in collagen gels. Extracellular signal-regulated kinase (Erk) 1/2, Akt and focal adhesion kinase (FAK) were activated by VEGF in HUVECs. The VEGF-induced expression of CRIM1 mRNA was significantly abrogated by PD98059 or PF562271, but was not affected by LY294002. These results demonstrate that CRIM1 is an early response gene in the presence of both angiogenic stimulation (VEGF) and environmental (extracellular matrix) factors, and Erk and FAK might be involved in the upregulation of CRIM1 mRNA expression in vascular endothelial cells.

Keywords: Angiogenesis; CRIM1; Endothelial; Erk; FAK.

MeSH terms

  • Bone Morphogenetic Protein Receptors
  • Cell Culture Techniques / methods
  • Chromones / pharmacology
  • Collagen
  • Endothelial Cells / cytology
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism*
  • Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Flavonoids / pharmacology
  • Focal Adhesion Kinase 1 / antagonists & inhibitors
  • Focal Adhesion Kinase 1 / metabolism
  • Gels
  • Gene Expression / drug effects
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Membrane Proteins / genetics*
  • Morpholines / pharmacology
  • Neovascularization, Physiologic / drug effects
  • Protein Kinase Inhibitors / pharmacology
  • Proto-Oncogene Proteins c-akt / antagonists & inhibitors
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA, Messenger / biosynthesis*
  • RNA, Messenger / genetics*
  • Signal Transduction / drug effects
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • CRIM1 protein, human
  • Chromones
  • Flavonoids
  • Gels
  • Membrane Proteins
  • Morpholines
  • Protein Kinase Inhibitors
  • RNA, Messenger
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
  • Collagen
  • Focal Adhesion Kinase 1
  • PTK2 protein, human
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases
  • Bone Morphogenetic Protein Receptors
  • 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one