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Tie1 deficiency induces endothelial–mesenchymal transition
Author(s) -
Garcia Julie,
Sandi Maria José,
Cordelier Pierre,
Binétruy Bernard,
Pouysségur Jacques,
Iovanna Juan Lucio,
Tournaire Roselyne
Publication year - 2012
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/embor.2012.29
Subject(s) - transition (genetics) , mesenchymal stem cell , microbiology and biotechnology , biology , genetics , gene
Endothelial–mesenchymal transition (EndMT) has a significant role in embryonic heart formation and in various pathologies. However, the molecular mechanisms that regulate EndMT induction remain to be elucidated. We show that suppression of receptor tyrosine kinase Tie1 but not Tie2 induces human endothelial cells to undergo EndMT and that Slug deficiency reverts this process. We find that Erk1/2, Erk5 and Akt cascades control Slug promoter activity induced by Tie1 deficiency. Interestingly, EndMT is present in human pancreatic tumour. We propose that EndMT associated with Tie1 downregulation participates in the pathological development of stroma observed in tumours.