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10.1038/cddis.2014.339 http://scihub22266oqcxt.onion/10.1038/cddis.2014.339 C4454314!4454314 !25118938     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25118938 &cmd=llinks): Failed to open stream: HTTP request failed! 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Detrimental effects of Notch1 signaling activated by cadmium in renal proximal tubular epithelial cells |pdf=|usr=}}{{25118938 }} gab.com Text Detrimental effects of Notch1 signaling activated by cadmium in renal proximal tubular epithelial cells JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=25118938 #FOAvip We examined the roles of Notch1 signaling and its cross-talk with other signaling pathways, including p53 and phosphatidylinositol-3-kinase (PI3K)/Akt, in cadmium-induced cellular damage in HK-2 human renal proximal tubular epithelial cells. Following exposure to cadmium chloride (CdCl2), the level of Notch intracellular domain (NICD), the cleaved form of the Notch1 receptor, was increased and accumulated in the nuclear fraction. Knockdown of Notch1 with siRNA or treatment with the ?-secretase inhibitor, DAPT (N-[N-(3,5-difluorophenacetyl-L-alanyl)]-S-phenylglycine t-butyl ester), prevented CdCl2-induced morphological change of HK-2 cells and reduction of cell viability. Knockdown of Jagged1 or Jagged2, the ligands of the Notch1 receptor, partially suppressed cadmium cytotoxicity. Inhibition of p53 activity with pifithrin-? or inhibition of PI3K with LY294002 suppressed CdCl2-induced cellular damage and elevation of Notch1-NICD. In addition, treatment with the epidermal growth factor receptor (EGFR) inhibitor, AG1478, and the insulin-like growth factor-1 receptor inhibitor, PPP, suppressed both Notch1-NICD accumulation and Akt phosphorylation in HK-2 cells exposed to CdCl2. However, knockdown of Notch1 did not affect CdCl2-induced p53 accumulation and phosphorylation but suppressed phosphorylation of EGFR, Akt, and p70 S6 kinase. Depletion of Notch1 suppressed CdCl2-induced reduction of E-cadherin expression and elevation of Snail expression. Furthermore, treatment with SB216763, an inhibitor of glycogen synthase kinase-3, suppressed the potency of LY294002 treatment to reduce Snail expression in HK-2 cells exposed to CdCl2. Knockdown of Snail with siRNA partially prevented HK-2 cells from CdCl2-induced reduction of E-cadherin expression and cellular damage. These results suggest that cadmium exposure induces the activation of Notch1 signaling in renal proximal tubular cells with cooperative activation by the p53 and PI3K/Akt signaling pathways; the resultant expression of Snail, a repressor of E-cadherin expression, might lead to cellular damage by decreasing cell-cell adhesion. Twit Text FOAVip Detrimental effects of Notch1 signaling activated by cadmium in renal proximal tubular epithelial cells ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=25118938 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25118938 #FOAvip English Wikipedia <ref>{{Cite pmid|25118938 }}</ref> Detrimental effects of Notch1 signaling activated by cadmium in renal proximal tubular epithelial cells #MMPMID25118938 Fujiki K ; Inamura H ; Matsuoka M Cell Death Dis 2014[Aug]; 5 (8 ): e1378 PMID25118938 show ga We examined the roles of Notch1 signaling and its cross-talk with other signaling pathways, including p53 and phosphatidylinositol-3-kinase (PI3K)/Akt, in cadmium-induced cellular damage in HK-2 human renal proximal tubular epithelial cells. Following exposure to cadmium chloride (CdCl2), the level of Notch intracellular domain (NICD), the cleaved form of the Notch1 receptor, was increased and accumulated in the nuclear fraction. Knockdown of Notch1 with siRNA or treatment with the ?-secretase inhibitor, DAPT (N-[N-(3,5-difluorophenacetyl-L-alanyl)]-S-phenylglycine t-butyl ester), prevented CdCl2-induced morphological change of HK-2 cells and reduction of cell viability. Knockdown of Jagged1 or Jagged2, the ligands of the Notch1 receptor, partially suppressed cadmium cytotoxicity. Inhibition of p53 activity with pifithrin-? or inhibition of PI3K with LY294002 suppressed CdCl2-induced cellular damage and elevation of Notch1-NICD. In addition, treatment with the epidermal growth factor receptor (EGFR) inhibitor, AG1478, and the insulin-like growth factor-1 receptor inhibitor, PPP, suppressed both Notch1-NICD accumulation and Akt phosphorylation in HK-2 cells exposed to CdCl2. However, knockdown of Notch1 did not affect CdCl2-induced p53 accumulation and phosphorylation but suppressed phosphorylation of EGFR, Akt, and p70 S6 kinase. Depletion of Notch1 suppressed CdCl2-induced reduction of E-cadherin expression and elevation of Snail expression. Furthermore, treatment with SB216763, an inhibitor of glycogen synthase kinase-3, suppressed the potency of LY294002 treatment to reduce Snail expression in HK-2 cells exposed to CdCl2. Knockdown of Snail with siRNA partially prevented HK-2 cells from CdCl2-induced reduction of E-cadherin expression and cellular damage. These results suggest that cadmium exposure induces the activation of Notch1 signaling in renal proximal tubular cells with cooperative activation by the p53 and PI3K/Akt signaling pathways; the resultant expression of Snail, a repressor of E-cadherin expression, might lead to cellular damage by decreasing cell-cell adhesion. |Cadmium Chloride/*toxicity [MESH] |Calcium-Binding Proteins/antagonists & inhibitors/genetics/metabolism [MESH] |Cell Line [MESH] |Chromones/pharmacology [MESH] |Down-Regulation/drug effects [MESH] |Epithelial Cells/cytology/drug effects/metabolism [MESH] |ErbB Receptors/antagonists & inhibitors/metabolism [MESH] |Humans [MESH] |Indoles/pharmacology [MESH] |Intercellular Signaling Peptides and Proteins/genetics/metabolism [MESH] |Jagged-1 Protein [MESH] |Jagged-2 Protein [MESH] |Kidney Tubules, Proximal/cytology [MESH] |Maleimides/pharmacology [MESH] |Membrane Proteins/antagonists & inhibitors/genetics/metabolism [MESH] |Morpholines/pharmacology [MESH] |Phosphatidylinositol 3-Kinases/metabolism [MESH] |Phosphoinositide-3 Kinase Inhibitors [MESH] |Phosphorylation/drug effects [MESH] |Quinazolines/pharmacology [MESH] |RNA Interference [MESH] |RNA, Small Interfering/metabolism [MESH] |Receptor, Notch1/antagonists & inhibitors/genetics/*metabolism [MESH] |Serrate-Jagged Proteins [MESH] |Signal Transduction/*drug effects [MESH] |Snail Family Transcription Factors [MESH] |Transcription Factors/antagonists & inhibitors/genetics/metabolism [MESH] |Tumor Suppressor Protein p53/metabolism [MESH]Detrimental effects of Notch1 signaling activated by cadmium in renal (epmc).pdf DeepDyve Pubget Overpricing