mrtfa inhibitor  (MedChemExpress)

Journal: Redox Biology

Article Title: Myo1f regulates monocyte adhesion and contributes to atherosclerosis via MRTFA-dependent ITGB2 expression

doi: 10.1016/j.redox.2026.104049

Figure Lengend Snippet: Myo1f promotes ITGB2 transcription through MRTFA. A, The adhesion of THP-1 cells to HUVECs after treatment with MRTFA knockdown lentivirus was observed under a fluorescence microscope (scale bar, 50 μm). Adherent cell numbers were calculated from 3 biological replicate images, and data are shown as fold change (ratio to shCtrl). B, Western blot analysis of MRTFA protein levels in THP-1 cells administered or not administered oxLDL (n = 3). C, Confirm the effectiveness of MRTFA knockdown lentivirus by western blotting (n = 3). D, Representative Western blot and quantification of ITGB2 expression after THP-1 knockdown of MRTFA with or without exposure to oxLDL (n = 3). E, Detection of Itgb2 mRNA levels of THP-1 under oxLDL stimulation by qPCR after elimination or not elimination of MRTFA (n = 5). F, Western blotting analysis of ITGB2 expression after gradient increase of MRTFA inhibitor CCG-1423 under oxLDL stimulation (n = 3). G, Representative confocal images of ITGB2 (red) with or without MRTFA knockdown and THP-1 stimulation with oxLDL (scale bar, 20 μm; n = 3). H, Western blot analysis of ITGB2 expression in oxLDL-stimulated THP-1 cells after overexpression of Myo1f with or without elimination of MRTFA (n = 3). I, Nuclear translocation of MRTFA following elimination of Myo1f based on oxLDL stimulation by dissociating cytoplasmic and nuclear analysis (n = 3). Data were presented as the mean ± SEM. Student's t-test (unpaired, two-tailed) for B, E and G . One-way ANOVA followed by Tukey's multiple comparisons test for A, C, D, F, H and I . Each P value is displayed in the image.

Article Snippet: Eight-week-old Apoe −/− mice were randomly divided into groups and simultaneously intraperitoneally injected with the MRTFA inhibitor (CCG-1423, 1 mg/kg, HY-13991, MCE) or vehicle and were given high-cholesterol feed for 8 weeks.

Techniques: Knockdown, Fluorescence, Microscopy, Western Blot, Expressing, Over Expression, Translocation Assay, Two Tailed Test

Journal: Redox Biology

Article Title: Myo1f regulates monocyte adhesion and contributes to atherosclerosis via MRTFA-dependent ITGB2 expression

doi: 10.1016/j.redox.2026.104049

Figure Lengend Snippet: Cytoskeletal polymerization promotes ITGB2 transcription and MRTFA nuclear translocation. A, Western blot analysis of ITGB2 expression after increasing gradient of G-actin polymerization inhibitor LAT-A under oxLDL stimulation (n = 3). B, The adhesion of THP-1 cells to HUVECs after treatment with LAT-A (2 μM) was observed under a fluorescence microscope (scale bar, 50 μm). Adherent cell numbers were calculated from 3 biological replicate images, and data are shown as fold change (ratio to DMSO). C, After overexpressing Myo1f and treating THP-1 cells with or without LAT-A, Western blot analysis was performed on ITGB2 expression under oxLDL stimulation (n = 3). D, Nuclear translocation of MRTFA after LAT-A treatment based on oxLDL stimulation by dissociated cytoplasmic and nuclear analysis (n = 3). E, Representative colocalization immunofluorescence micrographs of phalloidin-labeled F-actin (red) and Myo1f (green) staining in THP-1 cells. The scan line graph represents the F-actin and Myo1f staining intensity along the white straight line (scale bar, 20 μm; n = 3). F, By isolating F-actin and G-actin in THP-1 cells exposed to oxLDL with or without depletion of Myo1f, and quantifying their ratios by immunoblotting (n = 3). G, Effects of knockdown of Myo1f on MRTFA and actin binding in THP-1 cells. MRTFA antibody was used to co-immunoprecipitate actin in THP-1 cells with or without Myo1f knockdown treatment and stimulation with oxLDL (n = 3). Data were presented as the mean ± SEM. Student's t-test (unpaired, two-tailed) for F and G . One-way ANOVA followed by Tukey's multiple comparisons test for A-D . Each P value is displayed in the image.

Article Snippet: Eight-week-old Apoe −/− mice were randomly divided into groups and simultaneously intraperitoneally injected with the MRTFA inhibitor (CCG-1423, 1 mg/kg, HY-13991, MCE) or vehicle and were given high-cholesterol feed for 8 weeks.

Techniques: Translocation Assay, Western Blot, Expressing, Fluorescence, Microscopy, Immunofluorescence, Labeling, Staining, Knockdown, Binding Assay, Two Tailed Test

Journal: Redox Biology

Article Title: Myo1f regulates monocyte adhesion and contributes to atherosclerosis via MRTFA-dependent ITGB2 expression

doi: 10.1016/j.redox.2026.104049

Figure Lengend Snippet: Inhibiting MRTFA alleviates atherosclerosis. A, Schematic diagram of the intervention process by intraperitoneally injecting the MRTFA inhibitor CCG-1423 into Apoe −/− mice. B, Representative images of en face Oil Red O-stained aortas of Apoe −/− and Apoe −/− mice intraperitoneally injected with CCG-1423 are shown (n = 7). C, Representative images of HE and Oil Red O staining of cross-sections of aortic roots in mice with the indicated groups (scale bar, 200 μm; n = 7). D-F, Body weight and total plasma cholesterol and LDL-c levels in specific groups of mice (n = 7). G-I, The serum ALT, AST and Cr levels in specific groups of mice (n = 7). J, Western blot analysis of ITGB2 levels in mouse aortic plaques of mice in indicated groups (n = 7). K, Proposed mechanism of Myo1f in regulating monocyte adhesion and atherosclerosis progression. Data were presented as the mean ± SEM. Student's t-test (unpaired, two-tailed) for B-J . Each P value is displayed in the image.

Article Snippet: Eight-week-old Apoe −/− mice were randomly divided into groups and simultaneously intraperitoneally injected with the MRTFA inhibitor (CCG-1423, 1 mg/kg, HY-13991, MCE) or vehicle and were given high-cholesterol feed for 8 weeks.

Techniques: Staining, Injection, Clinical Proteomics, Western Blot, Two Tailed Test

Journal: Cell Death & Disease

Article Title: MKL1 promotes endothelial-to-mesenchymal transition and liver fibrosis by activating TWIST1 transcription

doi: 10.1038/s41419-019-2101-4

Figure Lengend Snippet: a Plasma ALT levels and AST levels. Expression levels of pro-fibrogenic genes were examined by qPCR ( b ) and Western ( c ). d Picrosirius red and Masson’s trichrome stainings. e Hepatic hydroxylproline levels. f Immunofluorescence staining was performed with anti-MKL1 (red) and anti-α-SMA (green). N = 4 mice for the sham groups and N = 8 mice for the BDL groups.

Article Snippet: In certain experiments, the mice were injected peritoneally the MKL1 inhibitor CCG-1423 (1 mg/kg, Selleck), the STAT3 inhibitor C188-9 (50 mg/kg, Selleck), or the TWIST1 inhibitor harmine (10 mg/kg, Selleck) daily after the BDL procedure.

Techniques: Clinical Proteomics, Expressing, Western Blot, Immunofluorescence, Staining

Journal: Cell Death & Disease

Article Title: MKL1 promotes endothelial-to-mesenchymal transition and liver fibrosis by activating TWIST1 transcription

doi: 10.1038/s41419-019-2101-4

Figure Lengend Snippet: Liver fibrosis was induced in WT or endothelial-specific MKL1 knockout (ecKO m/m ) mice by CCl 4 injection. Expression levels of pro-fibrogenic genes were examined by qPCR ( a ) and western ( b ). c Picrosirius red and Masson’s trichrome stainings. d Hepatic hydroxylproline levels. e Immunofluorescence staining was performed with anti-MKL1 (red) and anti-α-SMA (green). N = 4 mice for the sham groups and N = 6 mice for the BDL groups.

Article Snippet: In certain experiments, the mice were injected peritoneally the MKL1 inhibitor CCG-1423 (1 mg/kg, Selleck), the STAT3 inhibitor C188-9 (50 mg/kg, Selleck), or the TWIST1 inhibitor harmine (10 mg/kg, Selleck) daily after the BDL procedure.

Techniques: Knock-Out, Injection, Expressing, Western Blot, Immunofluorescence, Staining

Journal: Cell Death & Disease

Article Title: MKL1 promotes endothelial-to-mesenchymal transition and liver fibrosis by activating TWIST1 transcription

doi: 10.1038/s41419-019-2101-4

Figure Lengend Snippet: a Liver fibrosis was induced in WT or ecKO m/m mice by BDL. Primary sinusoidal endothelial cells were isolated and gene expression levels were examined by qPCR. b , c Human vascular endothelial cells were transfected with siRNA targeting MKL1 or scrambled siRNA (SCR) followed by treatment with TGF-β. Gene expression levels were examined by qPCR and western. d , e Human vascular endothelial cells were treated with TGF-β in the presence or absence of CCG-1423. Gene expression levels were examined by qPCR and western.

Article Snippet: In certain experiments, the mice were injected peritoneally the MKL1 inhibitor CCG-1423 (1 mg/kg, Selleck), the STAT3 inhibitor C188-9 (50 mg/kg, Selleck), or the TWIST1 inhibitor harmine (10 mg/kg, Selleck) daily after the BDL procedure.

Techniques: Isolation, Gene Expression, Transfection, Western Blot

Journal: Cell Death & Disease

Article Title: MKL1 promotes endothelial-to-mesenchymal transition and liver fibrosis by activating TWIST1 transcription

doi: 10.1038/s41419-019-2101-4

Figure Lengend Snippet: a Liver fibrosis was induced in WT or ecKO m/m mice by BDL. Primary sinusoidal endothelial cells were isolated and gene expression levels were examined by qPCR. b Human vascular endothelial cells were transfected with siRNA targeting MKL1 or scrambled siRNA (SCR) followed by treatment with TGF-β. TWIST1 expression levels were examined by qPCR and western. c TWIST1 promoter-luciferase constructs were transfected with or without MKL1 into HEK293 cells or EAhy926 cells. Luciferase activities were normalized by both GFP fluorescence and protein concentration. d Wild type or STAT3 mutant TWIST1 promoter-luciferase constructs were transfected with or without MKL1 into HEK293 cells or EAhy926 cells. Luciferase activities were normalized by both GFP fluorescence and protein concentration. e Human vascular endothelial cells were transfected with siRNA targeting STAT3 or scrambled siRNA (SCR) followed by treatment with TGF-β. ChIP assays were performed with indicated antibodies. f Co-immunoprecipitation was performed with indicated antibodies using lysates extracted from human vascular endothelial cells. g Human vascular endothelial cells were treated with TGF-β for 72 h. Cytoplasmic/nuclear proteins were extracted and blotted for MKL1 and STAT3. h Human vascular endothelial cells were treated with TGF-β for 72 h. Re-ChIP assays were performed with indicated antibodies.

Article Snippet: In certain experiments, the mice were injected peritoneally the MKL1 inhibitor CCG-1423 (1 mg/kg, Selleck), the STAT3 inhibitor C188-9 (50 mg/kg, Selleck), or the TWIST1 inhibitor harmine (10 mg/kg, Selleck) daily after the BDL procedure.

Techniques: Isolation, Gene Expression, Transfection, Expressing, Western Blot, Luciferase, Construct, Fluorescence, Protein Concentration, Mutagenesis, Immunoprecipitation

Journal: The Journal of Clinical Investigation

Article Title: Endothelial progerin expression causes cardiovascular pathology through an impaired mechanoresponse

doi: 10.1172/JCI121297

Figure Lengend Snippet: ( A ) Immunofluorescence of Wt and Prog-Tg ECs using MRTFA antibody and DAPI (images are representative of n = 3 independent experiments). Scale bar: 10 μm. ( B ) Representative confocal average intensity projections of Z stacks from mouse aorta of Wt and Prog-Tg animals stained with DAPI and MRTFA and progerin antibodies. EC nuclei (arrowheads) lie on internal elastic membrane that displays blue autofluorescence. Arrowheads, MRTFA-positive ECs. Note that MRTFA accumulates at the nuclear periphery of progerin-positive (white arrowheads) but not progerin-negative (yellow arrowheads) ECs ( n = 3 Wt and Prog-Tg littermate pairs). Scale bar: 10 μm. ( C ) Nos3 mRNA in Wt and Prog-Tg ECs after 24-hour treatment with 15 μM CCG-203971 MRTFA inhibitor or DMSO vehicle control. Values are normalized to Hprt and Nos3 / Hprt values in Prog-Tg cells are shown relative to values in Wt cells after MRTFA-inhibitor and control treatment. Nos3 / Hprt levels in Wt cells were arbitrary and set to 1 in both control and CCG-203971 conditions ( n = 5 independent experiments). Nos3 / Hprt levels in Prog-Tg cells relative to Wt are not significantly different (NS) after drug treatment, in contrast to control conditions ( P < 0.01). ( D ) Chromatin immunoprecipitation using anti-MRTFA or goat IgG control. Precipitated DNA was amplified by qPCR with primers spanning Nos3 promoter or gene body ( n = 3 independent experiments). ** P < 0.01 by unpaired Student’s t test ( C and D ). Data presented as mean ± SEM. ( E ) Acta2 levels normalized to Hprt in fibroblasts after 3 days of coculture with Wt and Prog-Tg ECs either left untreated (left) or treated with 25 μM MRTFA inhibitor CCG-203971 (right). Values were subtracted from those obtained in untreated or CCG-203971–treated fibroblast single cultures ( n = 6 Wt , n = 8 Prog-Tg , and n = 3 inhibitor-treated Prog-Tg samples). * P < 0.05 by Mann-Whitney U test. Data presented as median (middle line) with boxes encompassing 25th to 75th percentile, and whiskers, minimum to maximum values.

Article Snippet: On the second day, fibroblasts were either mock treated with DMSO or treated with the MRTFA inhibitor CCG-203971 (Tocris Bioscience).

Techniques: Immunofluorescence, Staining, Membrane, Chromatin Immunoprecipitation, Amplification, MANN-WHITNEY