c met inhibitor pha665752  (MedChemExpress)

Journal: Stem Cell Research & Therapy

Article Title: Paracrine stimulation of perinatal lung functional and structural maturation by mesenchymal stem cells

doi: 10.1186/s13287-020-02028-4

Figure Lengend Snippet: Growth factors were not responsible for the stimulating effect of MSC-CM on Na + transport. FDLE cells were subjected to MSC-CM or control medium for 24 h with or without the respective growth receptor inhibitor. Data are displayed as boxes and whiskers with the 10–90 percentiles, mean (+), and median (horizontal line). Statistical differences among groups were analyzed with an ANOVA and Tukey’s post hoc test. a Inhibition of VEGF-R with Axitinib ( n = 19–23, 2 IE; *** p < 0.001), b BMP-R with K02288 ( n = 22–24, 2 IE; *** p < 0.001), and c PDGF-R with AG-1296 ( n = 18–22, 2 IE; *** p < 0.001) did not affect Na + transport in MSC-CM-treated and control cells. d The EGF-R inhibitor AG-1478 ( n = 19–24, 2 IE; *** p < 0.001), e the TGF-β-R inhibitor SB431542 ( n = 21–24, 2 IE; * p < 0.05; *** p < 0.001), f the FGF-R inhibitor FIIN-2 ( n = 16–24, 2 IE; * p < 0.05; ** p < 0.01; *** p < 0.001), and g the HGF-R (c-met) inhibitor PHA665752 ( n = 64–67, 6 IE; ** p < 0.01; *** p < 0.001) reduced ∆ I amil in control and MSC-CM-treated cells. Inhibition did not prevent the stimulating effect of MSC-CM. □ control, ■ MSC-CM

Article Snippet: The inhibitors of the VEGF receptor (Axitinib, 10 μM), the bone morphogenetic protein receptor (BMP-R; K02288, 1 μM), the platelet-derived growth factor receptor (PDGF-R; AG-1296, 10 μM), the EGF receptor (EGF-R; AG-1478, 1 μM), the transforming growth factor β receptor (TGF-β-R; SB431542, 1 μM), the FGF receptor (FGF-R; FIIN-2, 1 μM), and the HGF receptor c-met (PHA665752, 1 μM) were purchased from Biomol (Hamburg, Germany).

Techniques: Control, Inhibition

Journal: Scientific Reports

Article Title: Proteomic analysis reveals a protective role of specific macrophage subsets in liver repair

doi: 10.1038/s41598-019-39007-6

Figure Lengend Snippet: Ly6C lo CX 3 CR1 hi macrophages directly accelerate hepatocyte proliferation in vitro . ( A ) Schematic of the experimental design. Normal hepatocytes (HCs) were co-cultured with the CM from 24 h Ly6C hi CX 3 CR1 lo macrophages or 72 h Ly6C lo CX 3 CR1 hi macrophages. ( B ) Representative images of hepatocytes pulsed with EdU and the quantification of hepatocyte proliferation are shown. Scale bar, 50 μm. ( C ) Differential expression of the indicated genes measured by qPCR in 24 h Ly6C hi CX 3 CR1 lo macrophages and 72 h Ly6C lo CX 3 CR1 hi macrophages, presented relative to Gapdh . ( D ) Hepatocytes were co-cultured with the CM from 72 h Ly6C lo CX 3 CR1 hi macrophages or supplemented with the c-Met kinase inhibitor PHA665752 (2.5 μM). Representative images of hepatocytes pulsed with EdU (left panel) and the quantification of hepatocyte proliferation (right panel) are shown. Scale bar, 50 μm. The data shown are representative of at least two independent experiments (n = 3/group). The results represent means ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001).

Article Snippet: Hepatocytes were treated with macrophage-derived CM or HGF (50 ng/ml, Peprotech) for 12 h, followed by EdU (5-ethynyl-2′-deoxyuridine, 20 μM) pulsing for an additional 36 h. In another series of experiments, isolated hepatocytes were treated with Ly6C lo CX 3 CR1 hi macrophage-derived CM supplemented with or without the c-Met kinase inhibitor PHA665752 (2.5 μM, R&D systems).

Techniques: In Vitro, Cell Culture, Quantitative Proteomics