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Tyrosine phosphatase beta regulates angiopoietin-Tie2 signaling in human endothelial cells Yacyshyn OK; Lai PF; Forse K; Teichert-Kuliszewska K; Jurasz P; Stewart DJAngiogenesis 2009[]; 12 (1): 25-33OBJECTIVES: The endothelial cell (EC)-selective receptor tyrosine kinase, Tie2, and its ligands angiopoietin Ang-1 and Ang-2, are essential for blood vessel maintenance and repair. Ang-1 is an agonist of Tie2 receptor activation, whereas Ang-2 is a context-dependent antagonist/agonist. Therefore, we investigated the role of the EC-selective phosphatase, human protein tyrosine phosphatase beta (HPTPbeta), in regulating Tie2 activity. METHODS AND RESULTS: siRNA silencing of HPTPbeta enhanced Ang-1 and Ang-2-induced Tie2 phosphorylation at 10 min (2.5-fold, P < 0.001; and 1.8-fold, P < 0.05, respectively). The cell survival response to Ang-1, but not Ang-2, was enhanced by HPTPbeta silencing as measured by flow cytometry (0.85-fold to 0.66-fold, P < 0.05) and ELISA (0.88-fold to 0.53-fold, P < 0.01). Hypoxia, which upregulated HPTPbeta expression in endothelial cells, impaired Ang-1-induced Tie2 phosphorylation. CONCLUSIONS: These results reveal a novel role for HPTPbeta in modulating Ang-1-Tie2 signaling and endothelial cell survival.|*Signal Transduction/drug effects[MESH]|Angiopoietin-1/pharmacology[MESH]|Angiopoietin-2/pharmacology[MESH]|Angiopoietins/*metabolism/pharmacology[MESH]|Cell Hypoxia/drug effects[MESH]|Cell Movement/drug effects[MESH]|Cell Survival/drug effects[MESH]|Cells, Cultured[MESH]|Endothelial Cells/cytology/drug effects/*enzymology[MESH]|Gene Expression Regulation, Enzymologic/drug effects[MESH]|Humans[MESH]|Phosphorylation/drug effects[MESH]|RNA, Messenger/genetics/metabolism[MESH]|RNA, Small Interfering/metabolism[MESH]|Receptor, TIE-2/*metabolism[MESH]|Receptor-Like Protein Tyrosine Phosphatases, Class 5/antagonists & inhibitors/genetics/*metabolism[MESH]|Vanadates/pharmacology[MESH] |
