mouse anti-ho1 antibody  (Thermo Fisher)

Journal: Journal of Inflammation (London, England)

Article Title: Esomeprazole attenuates inflammatory and fibrotic response in lung cells through the MAPK/Nrf2/HO1 pathway

doi: 10.1186/s12950-021-00284-6

Figure Lengend Snippet: Western blot data showing increased expression of heme oxygenase 1 (HO1) protein by esomeprazole in human IPF lung fibroblasts. The cells were treated with esomeprazole (1–100 μM) for 24 h prior to isolation of total protein. Data is representative of three independent experiments. Beta actin (ACTB) is used as a loading control. Cont = control. * p < 0.05 vs control (cont)

Article Snippet: Human lung epithelial cells were cultured in 6-well plates until 70% confluency and incubated further in the absence or presence of esomeprazole (1–100 μM) for 24 h. The cells were fixed with paraformaldehyde (4%) and permeabilized with 0.1% triton-X100 for 15 min prior to staining for HO1 using mouse anti-HO1 antibody (ThermoFisher; cat # MA1–112; 1:100).

Techniques: Western Blot, Expressing, Isolation, Control

Journal: Journal of Inflammation (London, England)

Article Title: Esomeprazole attenuates inflammatory and fibrotic response in lung cells through the MAPK/Nrf2/HO1 pathway

doi: 10.1186/s12950-021-00284-6

Figure Lengend Snippet: Quantitative RT-PCR (qRT-PCR) data showing upregulation of pro-inflammatory molecules TNFα, IL-1β and IL-6 in primary human lung epithelial cells treated with bleomycin for 24 h. The data also shows that treatment with esomeprazole significantly downregulated induction of the inflammatory molecules while inhibition of heme oxygenase 1 (HO1) with its selective inhibitor Tin protoporphyrin IX (SnPPIX; 1 μM) impaired the effect of esomeprazole on the expression of the inflammatory molecules. Data is Mean ± SEM from triplicate experiments. * p < 0.05 between bleomycin only vs. bleomycin + esomeprazole. ** p < 0.05 between bleomycin + esomeprazole vs. bleomycin + esomeprazole + SnPPIX

Article Snippet: Human lung epithelial cells were cultured in 6-well plates until 70% confluency and incubated further in the absence or presence of esomeprazole (1–100 μM) for 24 h. The cells were fixed with paraformaldehyde (4%) and permeabilized with 0.1% triton-X100 for 15 min prior to staining for HO1 using mouse anti-HO1 antibody (ThermoFisher; cat # MA1–112; 1:100).

Techniques: Quantitative RT-PCR, Inhibition, Expressing

Journal: Journal of Inflammation (London, England)

Article Title: Esomeprazole attenuates inflammatory and fibrotic response in lung cells through the MAPK/Nrf2/HO1 pathway

doi: 10.1186/s12950-021-00284-6

Figure Lengend Snippet: a Gene expression data showing upregulation of heme oxygenase 1 (HO1) by esomeprazole (100 μM) in human IPF lung fibroblasts. The data also shows that selective inhibition of nuclear factor-like 2 (Nrf2) with trigonelline (1 μM) impaired the induction of HO1 by esomeprazole. * p < 0.05 compared to esomeprazole alone. b Genetic deletion of Nrf2 (Nrf2−/−) impaired activation of HO1 by esomeprazole. Lung fibroblasts from Nrf2−/− mice were incubated with esomeprazole for 1–6 h. ACTB is used as a loading control. Crtl = control. Data is representative of three independent experiments

Article Snippet: Human lung epithelial cells were cultured in 6-well plates until 70% confluency and incubated further in the absence or presence of esomeprazole (1–100 μM) for 24 h. The cells were fixed with paraformaldehyde (4%) and permeabilized with 0.1% triton-X100 for 15 min prior to staining for HO1 using mouse anti-HO1 antibody (ThermoFisher; cat # MA1–112; 1:100).

Techniques: Gene Expression, Inhibition, Activation Assay, Incubation, Control

Journal: Journal of Inflammation (London, England)

Article Title: Esomeprazole attenuates inflammatory and fibrotic response in lung cells through the MAPK/Nrf2/HO1 pathway

doi: 10.1186/s12950-021-00284-6

Figure Lengend Snippet: Gene expression data showing upregulation of heme oxygenase 1 (HO1) by esomeprazole (100 μM) in human IPF lung fibroblasts. The data also shows that selective inhibition of MAP-ERK kinase 1/2 (MEK1/2) with U0126 (10 μM) impaired the induction of HO1 by esomeprazole. Data is Mean ± SEM from duplicate experiments. * p < 0.05 compared to esomeprazole alone

Article Snippet: Human lung epithelial cells were cultured in 6-well plates until 70% confluency and incubated further in the absence or presence of esomeprazole (1–100 μM) for 24 h. The cells were fixed with paraformaldehyde (4%) and permeabilized with 0.1% triton-X100 for 15 min prior to staining for HO1 using mouse anti-HO1 antibody (ThermoFisher; cat # MA1–112; 1:100).

Techniques: Gene Expression, Inhibition

Journal: Journal of Inflammation (London, England)

Article Title: Esomeprazole attenuates inflammatory and fibrotic response in lung cells through the MAPK/Nrf2/HO1 pathway

doi: 10.1186/s12950-021-00284-6

Figure Lengend Snippet: Signal transduction involving growth factors, receptor tyrosine kinases and members of the MAP kinase family. Esomeprazole-mediated activation of heme oxygenase 1 (HO1) involving phosphorylation of MEK, ERK and translocation of Nrf2 to control pro-inflammatory and profibrotic processes is illustrated

Article Snippet: Human lung epithelial cells were cultured in 6-well plates until 70% confluency and incubated further in the absence or presence of esomeprazole (1–100 μM) for 24 h. The cells were fixed with paraformaldehyde (4%) and permeabilized with 0.1% triton-X100 for 15 min prior to staining for HO1 using mouse anti-HO1 antibody (ThermoFisher; cat # MA1–112; 1:100).

Techniques: Transduction, Activation Assay, Phospho-proteomics, Translocation Assay, Control