scholarly journals Erratum to: AGE-RAGE interaction in the TGFβ2-mediated epithelial to mesenchymal transition of human lens epithelial cells

2016 ◽  
Vol 33 (5) ◽  
pp. 837-838
Author(s):  
Cibin T. Raghavan ◽  
Ram H. Nagaraj
Keyword(s):  
Epithelial Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Mesenchymal Transition ◽  
Human Lens Epithelial Cells

Ganglioside GM3 participates in the TGF-β1-induced epithelial–mesenchymal transition of human lens epithelial cells

2012 ◽  
Vol 449 (1) ◽  
pp. 241-251 ◽  
Author(s):  
Seok-Jo Kim ◽  
Tae-Wook Chung ◽  
Hee-Jung Choi ◽  
Choong-Hwan Kwak ◽  
Kwon-Ho Song ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Ganglioside Gm3 ◽  
Mesenchymal Transition ◽  
Human Lens Epithelial Cells ◽  
Gm3 Synthase ◽  
Tgf Β1

TGF-β (transforming growth factor-β)-induced EMT (epithelial–mesenchymal transition) induces the proliferation and migration of the HLE (human lens epithelial) cells. Ganglioside GM3, simple sialic-acid-containing glycosphingolipids on mammalian cell membranes, regulates various pathological phenomena such as insulin resistance and tumour progression. However, the relationship between ganglioside GM3 and TGF-β-induced EMT in the HLE B-3 cells is poorly understood. In the present study we demonstrated that ganglioside GM3 was involved in TGF-β1-induced EMT in HLE B-3 cells. Our results indicated that the expression of ganglioside GM3 and GM3 synthase mRNA were significantly increased in TGF-β1-induced HLE B-3 cells. Reporter gene analysis also demonstrated that transcriptional activation of the GM3 synthase gene was regulated by Sp1 (specificity protein 1) in HLE B-3 cells upon TGF-β1 stimulation. Interestingly, the inhibition of ganglioside GM3 expression by d-PDMP [d-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol] and GM3 synthase shRNA (short hairpin RNA) resulted significantly in the suppression of cell migration and EMT-related signalling in HLE B-3 cells stimulated by TGF-β. Furthermore, exogenous treatment of ganglioside GM3 rescued the expression of EMT molecules and cell migration suppressed by the depletion of ganglioside GM3 in TGF-β1-induced HLE B-3 cells. We also found that ganglioside GM3 interacted with TGFβRs (TGF-β receptors) in TGF-β1-induced HLE B-3 cells. Taken together, these results suggest that ganglioside GM3 induced by TGF-β1 regulates EMT by potential interaction with TGFβRs.

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