Journal: British Journal of Pharmacology

Article Title: Characterization of the properties of a selective, orally bioavailable autotaxin inhibitor in preclinical models of advanced stages of liver fibrosis

doi: 10.1111/bph.14118

Figure Lengend Snippet: Biochemical quantification of hepatic hydroxyproline (HYP) content and αSMA in models of chronic liver injury in rats. (A) Hepatic HYP content in control, CCl4/Vehicle‐ and CCl4/Ex_31‐treated rats. (B) Hepatic αSMA content in control, CCl4/Vehicle‐ and CCl4/Ex_31‐treated rats. (C) Hepatic HYP content in CSAA or CDAA diet‐fed rats treated with Vehicle or Ex_31. (D) Hepatic αSMA content in CSAA or CDAA diet‐fed rats treated with Vehicle or Ex_31. Values are normalized versus liver protein content. Data represent mean ± SEM, n = 10 (control), n = 13 (CCl4‐treated) and n = 12 (CSAA‐ and CDAA‐fed), *P < 0.05.

Article Snippet: An MSD Western‐replacement method (Meso Scale Discovery) using specific anti‐α smooth muscle actin (αSMA) antibody was used to quantify SMA in protein lysates.

Techniques: Control

Journal: Stem Cells Translational Medicine

Article Title: Extracellular Vesicles From Mesenchymal Umbilical Cord Cells Exert Protection Against Oxidative Stress and Fibrosis in a Rat Model of Bronchopulmonary Dysplasia

doi: 10.1093/stcltm/szad070

Figure Lengend Snippet: Antibody list.

Article Snippet: FITC mouse anti-αSMA , GTX72531 , Genetex.

Techniques:

Journal: Frontiers in Aging Neuroscience

Article Title: Nimodipine augments cerebrovascular reactivity in aging but runs the risk of local perfusion reduction in acute cerebral ischemia

doi: 10.3389/fnagi.2023.1175281

Figure Lengend Snippet: Immunocytochemical characterization of cerebrovascular smooth muscle cell (cerebrovascular SMC) senescence. (A) Representative fluorescence micrographs of αSMA and p16 co-localization (arrows) in the hippocampal CA1 region of an old animal. αSMA corresponding to cerebrovascular SMC coverage is shown in green, p16 labeling indicating senescent cells is red; and DAPI illustrates the cell nuclei in blue. (B) Relative area covered by cerebrovascular SMC labeled with αSMA in different forebrain regions in young and old animals. (C) The number of senescent cerebrovascular SMCs in young and old animals in different brain regions. Individual data points represent the mean value of three sections in each animal. Bar charts show mean ± stdev. The normal distribution of data was evaluated with a Shapiro–Wilk test ( B : p = 0.488, C : p = 0.709). For further statistical analysis, a repeated measures model was used (RM ANOVA), followed by a Holm Sidak post hoc test. Levels of significance were set as p < 0.05 * , p < 0.01 ** , p < 0.001 *** vs. Young vehicle.

Article Snippet: Cerebrovascular SMCs were labeled with alpha smooth muscle actin (αSMA) immunostaining (monoclonal primary anti-αSMA antibody produced in mouse, Genetex, U.S.A., GTX73419, 1 h).

Techniques: Fluorescence, Labeling

Journal: Frontiers in Aging Neuroscience

Article Title: Nimodipine augments cerebrovascular reactivity in aging but runs the risk of local perfusion reduction in acute cerebral ischemia

doi: 10.3389/fnagi.2023.1175281

Figure Lengend Snippet:

Article Snippet: Cerebrovascular SMCs were labeled with alpha smooth muscle actin (αSMA) immunostaining (monoclonal primary anti-αSMA antibody produced in mouse, Genetex, U.S.A., GTX73419, 1 h).

Techniques: Saline

Journal: EMBO Reports

Article Title: TLR4‐dependent shaping of the wound site by MSCs accelerates wound healing

doi: 10.15252/embr.201948777

Figure Lengend Snippet: Representative photomicrographs of confocal microscopy of sections from differently injected day 1 wounds stained for Ly6G + neutrophils (green) and F4/80 + macrophages (red). Nuclei are stained with DAPI (blue). Double staining was performed for sections of day 1 wounds injected with PBS (control), non‐primed MSCs, LPS‐primed MSCs, and LPS‐primed TLR4‐silenced MSCs. Double‐stained cells indicate phagocytic engulfment of neutrophils by macrophages. To facilitate comparison, areas inside the rectangles are shown at 5× magnification in the insets. Scale bar: 100 μm. Quantification of Ly6G and F4/80 double‐positive cells on sections of differently injected day 1 wounds. Wounds were injected as described in (A). Double‐positive cells were counted; statistical analysis was performed using one‐way ANOVA, and values are represented as mean ± SEM, six biological replicates. Quantification of Ly6G + neutrophils and F4/80 + macrophages on sections of differently injected day 1 wounds. Wounds were injected as described in (A). Single‐positive cells were counted; statistical analysis was performed using one‐way ANOVA, and values are represented as mean ± SEM, six biological replicates. Representative photomicrographs of confocal microscopy of sections from differently injected day 3 wounds double‐stained for TGFβ‐1 (red) and for F4/80 + macrophages (green). Nuclei are stained with DAPI (blue). Double staining was performed for sections of day 5 wounds injected with PBS (control), non‐primed MSCs, LPS‐primed MSCs, and LPS‐primed TLR4‐silenced MSCs. Scale bar: 50 μm. Representative photomicrographs of sections of day 5 wounds immunostained for CD31 (indicative of endothelial cells and newly formed vessels) and for α‐SMA (indicative of myofibroblasts differentiation) after injection of LPS‐primed MSCs, non‐primed MSCs, LPS‐primed TLR4‐silenced MSCs or PBS (middle and lower panel). To facilitate comparison, areas inside the rectangles are shown at 5× magnification in the insets. Scale bars: 50 μm. Double‐positive macrophages stained for TGFβ‐1 and F4/80 were counted; statistical analysis was performed using one‐way ANOVA, and values are represented as mean ± SEM, six biological replicates. Quantitative analysis of CD31‐positive endothelial cells in sections of wounds injected with PBS, non‐primed MSCs, LPS‐primed MSCs, and LPS‐primed TLR4‐silenced LPS. Cell counting was performed on immunostained wound sections; statistical analysis was performed using one‐way ANOVA, and values are represented as mean ± SEM, six biological replicates. Western blot analysis of lysates from day 5 wounds (left panel) and the corresponding densitometric analysis (right panel) depict enhanced α‐SMA protein expression in wounds injected with LPS‐primed MSCs as opposed to the respective control groups. Actin served as loading control. Statistical analysis was performed using one‐way ANOVA, and values are represented as mean ± SEM, three biological replicates. Source data are available online for this figure.

Article Snippet: In addition, we employed primary antibodies against α‐SMA (Progen), CD206 (Biorbyt), CXCL5 (Gene Tex), CXCL6 (Biorbyt), IL‐1β (Abcam), IL‐6 (R&D), IL‐8 (R&D), β2M (Signaling), F4/80 (eBioscience), TGFβ‐1 and CD31 (Cell Signaling), MIP2/KC and GCSF (R&D), and LIX (Biorbyt).

Techniques: Confocal Microscopy, Injection, Staining, Double Staining, Control, Comparison, Cell Counting, Western Blot, Expressing