PUBLICATION
Angiomotin-like2 Gene (amotl2) Is Required for Migration and Proliferation of Endothelial Cells during Angiogenesis
- Authors
- Wang, Y., Li, Z., Xu, P., Huang, L., Tong, J., Huang, H., and Meng, A.
- ID
- ZDB-PUB-111011-1
- Date
- 2011
- Source
- The Journal of biological chemistry 286(47): 41095-104 (Journal)
- Registered Authors
- Meng, Anming, Tong, Jingyuan, Xu, Pengfei
- Keywords
- angiogenesis, embryo, endothelial cell, MAP kinases (MAPKs), zebrafish angiomotion-like2
- MeSH Terms
-
- Carrier Proteins/chemistry
- Carrier Proteins/genetics
- Carrier Proteins/metabolism*
- Zebrafish Proteins/chemistry
- Zebrafish Proteins/deficiency
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- Cell Polarity/genetics
- Extracellular Signal-Regulated MAP Kinases/metabolism
- Human Umbilical Vein Endothelial Cells/cytology
- Human Umbilical Vein Endothelial Cells/metabolism
- Gene Knockdown Techniques
- Enzyme Activation/genetics
- Amino Acid Motifs
- Cell Proliferation
- Mice
- Phosphorylation/genetics
- Endothelial Cells/cytology*
- Endothelial Cells/metabolism*
- Cell Movement*/genetics
- Neovascularization, Physiologic*/genetics
- Blood Vessels/cytology
- Blood Vessels/physiology
- HEK293 Cells
- Signal Transduction/genetics
- src-Family Kinases
- Protein-Tyrosine Kinases/metabolism
- Zebrafish/embryology
- Membrane Proteins/chemistry
- Membrane Proteins/deficiency
- Membrane Proteins/genetics
- Membrane Proteins/metabolism*
- Humans
- Animals
- Tyrosine/metabolism
- PubMed
- 21937427 Full text @ J. Biol. Chem.
Citation
Wang, Y., Li, Z., Xu, P., Huang, L., Tong, J., Huang, H., and Meng, A. (2011) Angiomotin-like2 Gene (amotl2) Is Required for Migration and Proliferation of Endothelial Cells during Angiogenesis. The Journal of biological chemistry. 286(47):41095-104.
Abstract
Angiogenesis involves sprouting, migration and proliferation of endothelial cells. angiomotin-like2 (amotl2) has been found to express in blood vessels in zebrafish embryos, but its function in angiogenesis and underlying mechanisms remain unknown. In this study, we demonstrate that knockdown of amotl2 in zebrafish Tg(fli1:EGFP)y1 and Tg(fli1:nEGFP)y7 transgenic embryos impairs the intersegmental vessel (ISV) growth and suppresses proliferation of endothelial cells. Transplantation experiments indicate that function of amotl2 in ISV growth is cell-autonomous. AMOTL2 knockdown in cultured human umbilical vein endothelial cells (HUVECs) also inhibits cell proliferation and migration and disrupts cell polarity, ultimately interrupting the formation of vascular tube-like structures. Amotl2 promotes MAPK/ERK activation via c-Src, which is dependent on phosphorylation of tyrosine residue at position 103 but independent of C-terminal PDZ-binding domain. Taking together, our data indicate that Amotl2 plays a pivotal role in polarity, migration and proliferation of angiogenic endothelial cells.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping