Journal: Cytotechnology

Article Title: TGF-β1 signaling activates hepatic stellate cells through Notch pathway

doi: 10.1007/s10616-019-00329-y

Figure Lengend Snippet: Inhibition of HSCs transformation into MFs by Notch pathway inhibitor LY450139. a mRNA expression of Notch pathway marker Notch1 and α-SMA were examined by qRT-PCR. mRNA expression of Notch1 and α-SMA was evidently decreased in HSCs after treating with LY450139 for 48 h compared to those in TGF-β1-stimualted and control HSCs. b Protein expression of Notch1 and α-SMA was tested by western blotting. Expression of Notch1 and α-SMA proteins was also distinctly downregulated after inhibiting Notch pathway in HSCs. ***p < 0.01 and *p < 0.05 compared with the control group respectively; Scale bars = mean ± SEM, n = 3/group

Article Snippet: The activation group and control group HSCs were treated with specific Notch pathway inhibitor LY450139 (10 μM; Abmole Bioscience Inc, USA) at the same time for 48 h to determine the effect of Notch pathway on HSCs activation process.

Techniques: Inhibition, Transformation Assay, Expressing, Marker, Quantitative RT-PCR, Control, Western Blot

Journal: Cell Death & Disease

Article Title: Akt2 mediates glucocorticoid resistance in lymphoid malignancies through FoxO3a/Bim axis and serves as a direct target for resistance reversal

doi: 10.1038/s41419-018-1043-6

Figure Lengend Snippet: a Levels of apoptosis of cells treated with different concentrations of the Akt inhibitor or different concentrations of Akt inhibitor combined with DEX were measured using flow cytometry. b , c Apoptosis was measured by flow cytometry in CCRF-CEM cells treated with ethanol, DEX (1 µM), Akt inhibitor (1 µM), PI3K inhibitor LY294002 (30 µM), Akt inhibitor (1 µM) plus ethanol, LY294002 (30 µM) plus ethanol, Akt inhibitor (1 µM) plus DEX (1 µM) or LY294002 (30 µM) plus DEX (1 µM). d Levels of p-FoxO3a and Bim in CCRF-CEM cells treated with ethanol, DEX, Akt inhibitor, PI3K inhibitor, LY294002 or a combination of the inhibitors were examined by western blot with the indicated antibodies. GAPDH served as a loading control. e Apoptosis analysis using flow cytometry in CCRF-CEM T-ALL cells treated with the glycolysis inhibitor 2-DG (2 mM), DEX (1 µM) or 2-DG (2 mM) plus DEX (1 µM). f Relative levels of FoxO3a/Bim signaling proteins in CCRF-CEM cells treated with the glycolysis inhibitor 2-DG (2 mM), DEX (1 µM) or 2-DG (2 mM) plus DEX (1 µM) as measured by western blot. Levels were normalized to GAPDH. g Analysis of FoxO3a and p-FoxO3a (Ser253) levels in CCRF-CEM cells treated with the notch signaling inhibitor dapt (20 µM), DEX (1 µM) or dapt (20 µM) plus DEX (1 µM) by western blot. GAPDH served as a loading control. h Analysis of apoptosis using flow cytometry in CCRF-CEM T-ALL cells treated with the notch signaling inhibitor dapt (20 µM), DEX (1 µM) or dapt (20 µM) plus DEX (1 µM). i Analysis of apoptosis using flow cytometry in CCRF-CEM T-ALL cells, L1210 leukemia cells from mice, Raji or Daudi Burkitt’s lymphoma cells treated with ethanol plus vehicle, SGK inhibitor GSK (1, 5 µM) plus ethanol, vehicle plus DEX or GSK (1, 5 µM) plus DEX. j Analysis of apoptosis by flow cytometry in CCRF-CEM T-ALL cells treated with different pathway inhibitors including GSK, dapt, 2-DG, LY294002 and Akt IV combined with DEX (1 µM). k Apoptosis was measured by flow cytometry in Jurkat T-ALL cells, Molt-4 T-ALL cells, SP2/0 myeloma cells from mice or Raji Burkitt’s lymphoma cells treated with DMSO only, Akt inhibitor (1 µM), DEX or Akt inhibitor (1 µM) combined with DEX. Bar graphs in c , f , g – k represent mean ± SD

Article Snippet: Levels were normalized to GAPDH. g Analysis of FoxO3a and p-FoxO3a (Ser253) levels in CCRF-CEM cells treated with the notch signaling inhibitor dapt (20 μM), DEX (1 μM) or dapt (20 μM) plus DEX (1 μM) by western blot.

Techniques: Flow Cytometry, Western Blot, Control