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Human Embryonic Stem Cells Maintain Pluripotency after E‐Cadherin Expression Knockdown
Author(s) -
Byas Shanel Nicole,
Klim Joseph,
Kiessling Laura
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb172
Subject(s) - microbiology and biotechnology , gene knockdown , cadherin , rna interference , embryonic stem cell , lipofectamine , biology , cellular differentiation , induced pluripotent stem cell , transfection , stem cell , chemistry , cell , cell culture , gene , rna , genetics , recombinant dna , vector (molecular biology)
E‐cadherin is a Ca2+‐dependent adhesion molecule essential for cell‐cell interaction [1]. E‐cadherin has been reported to have a crucial role in cellular migration, proliferation, differentiation, and the maintenance of tissue integrity [1]. The down‐regulation of E‐cadherin in cells has been shown to be associated with the epithelial‐mesenchymal transition of tissues and apoptosis, leading to the assumption that E‐cadherin is critical to cellular survival and pluripotential [2]. On the basis of this assumption, two RNA interference (RNAi) transfection reagents, Lipofectamine ™ RNAiMax Reagent (Invitrogen®) and Accell™ siRNA Delivery (Thermo Scientific Dharmacon®), were used to decrease the gene expression of E‐cadherin in H9 stem cell lines to determine the signaling pathways of cellular differentiation. The results reveal that although E‐cadherin gene expression in H9 stem cells decreased after RNAi knockdown, the cells remained pluripotent. These results refute prior claims that the presence of E‐cadherin is crucial for cellular differentiation and imply that the down‐regulation of E‐cadherin is not associated with the epithelial‐mesenchymal transition of tissues and apoptosis. E‐cadherin may not be critical to cellular survival and pluripotential, providing a basis for more extensive research on signaling pathways of differentiation. Supported by NIH T34GM008411