Journal: Experimental & molecular medicine

Article Title: Loss of KDM5B ameliorates pathological cardiac fibrosis and dysfunction by epigenetically enhancing ATF3 expression.

doi: 10.1038/s12276-022-00904-y

Figure Lengend Snippet: Fig. 2 KDM5B deficiency protects the heart from dysfunction and adverse cardiac remodeling after MI. a Echocardiographic measurement of the LVEF, LVFS, left ventricular end-diastolic internal dimension (LVIDd), and left ventricular end-systolic internal dimension (LVIDs) of KDM5B-KO or WT mice at baseline (Day 0) and on the indicated day after MI or sham operation (n = 6 mice per group). b–e Representative Masson’s trichrome staining images and quantitation of the scar size (b, c) or Sirius red staining images and quantitation of the fibrosis area (d, e) in myocardial tissues from KDM5B-KO or WT mice on Day 28 after MI. n = 6 mice per group. Scale bar, 1.6 mm (upper), 200 μm (bottom). f Q-PCR analysis of Col1a1 and Col3a1 mRNA levels in myocardial tissues from KDM5B-KO or WT mice on Day 14 after MI or sham operation (n = 6 mice per group). g Representative immunofluorescence staining of α-SMA (red) and Col III (green) in myocardial tissues from KDM5B-KO or WT mice on Day 14 after MI (n = 6 mice per group). Scale bar, 50 μm. *p < 0.05, **p < 0.01, ***p < 0.001. Unpaired Student’s t test (c, e) or ANOVA (a, f) was performed.

Article Snippet: Antibodies against collagen type III (NB600-594) were obtained from Novus Biologicals (Littleton, CO).

Techniques: Staining, Quantitation Assay

Journal: Experimental & molecular medicine

Article Title: Loss of KDM5B ameliorates pathological cardiac fibrosis and dysfunction by epigenetically enhancing ATF3 expression.

doi: 10.1038/s12276-022-00904-y

Figure Lengend Snippet: Fig. 3 KDM5B deficiency prevents pressure overload-induced cardiac dysfunction and cardiac fibrosis. a Representative echocardio- graphic M-mode images of left ventricles from KDM5B-KO or littermate control WT mice on Day 28 after AngII or normal saline (NS) infusion. b, c Echocardiographic measurement of the LVEF (b) and LVFS (c) of KDM5B-KO or WT mice on Day 28 after AngII or NS infusion (n = 6 mice per group). d, e The ratio of heart weight to body weight (HW/BW) (d) and the ratio of heart weight to tibia length (HW/TL) (e) of KDM5B-KO or WT mice on Day 28 after AngII or NS infusion (n = 6 mice per group). f–i Representative Masson’s trichrome images and quantitation of perivascular (f, g) or interstitial (h, i) fibrosis in myocardial tissues from KDM5B-KO or WT mice on Day 28 after AngII or NS infusion (n = 6 mice per group). Scale bar, 200 μm (left), 100 μm (right). j Q-PCR analysis of Acta2, Col1a1, Col3a1 and Ctgf mRNA expression levels in myocardial tissues from KDM5B-KO or WT mice on Day 28 after AngII or NS infusion (n = 6 mice per group). k Immunoblot analysis of Col I and Col III protein expression in myocardial tissues from KDM5B-KO or WT mice on Day 28 after AngII or NS infusion. l Representative immunofluorescence staining of α-SMA (red) and Col III (green) in myocardial tissues from KDM5B-KO or WT mice on Day 28 after AngII infusion. Scale bar, 50 μm. *p < 0.05, **p < 0.01. Unpaired Student’s t test (g, i) or one-way ANOVA (b–e, j) was performed.

Article Snippet: Antibodies against collagen type III (NB600-594) were obtained from Novus Biologicals (Littleton, CO).

Techniques: Control, Saline, Quantitation Assay, Expressing, Western Blot, Staining

Journal: Experimental & molecular medicine

Article Title: Loss of KDM5B ameliorates pathological cardiac fibrosis and dysfunction by epigenetically enhancing ATF3 expression.

doi: 10.1038/s12276-022-00904-y

Figure Lengend Snippet: Fig. 4 KDM5B promotes fibrotic responses and the transition of cardiac fibroblasts. a, b Q-PCR analysis of Col1a1, Col3a1, Fn1 and Ccn2 mRNA expression (a) (n = 6 per group) or immunoblot analysis of Col I and Col III protein expression (b) in KDM5B-deficient (KO) or littermate control WT cardiac fibroblasts stimulated with TGF-β (10 ng/ml) for 24 h. c, d Q-PCR analysis of Col1a1, Col3a1, Fn1 and Ccn2 mRNA expression (c) (n = 6 per group) or immunoblot analysis of Col I and Col III protein expression (d) in Kdm5b-silenced or control siRNA-transfected cardiac fibroblasts stimulated with TGF-β (10 ng/ml) for 24 h. e, f Q-PCR analysis of Col1a1, Col3a1, Fn1 and Ccn2 mRNA expression (e) (n = 6 per group) or immunoblot analysis of Col I and Col III protein expression (f) in cardiac fibroblasts treated with the KDM5B inhibitor GSK467 or DMSO followed by stimulation with TGF-β (10 ng/ml) for 24 h. g–i Representative immunofluorescence staining of α-SMA (red) in cardiac fibroblasts with KDM5B-deficiency (g), KDM5B knockdown (h) or GSK467 treatment (i) and the corresponding control cardiac fibroblasts (g–i) stimulated with TGF-β (10 ng/ml) for 24 h. Similar results were obtained from three independent experiments (g–i). Scale bar, 50 μm. *p < 0.05, **p < 0.01, ***p < 0.001. Unpaired Student’s t test (a, c, e) was performed.

Article Snippet: Antibodies against collagen type III (NB600-594) were obtained from Novus Biologicals (Littleton, CO).

Techniques: Expressing, Western Blot, Control, Transfection, Staining, Knockdown

Journal: Cell reports

Article Title: Epigenetic Reprogramming of Cancer-Associated Fibroblasts Deregulates Glucose Metabolism and Facilitates Progression of Breast Cancer

doi: 10.1016/j.celrep.2020.107701

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: The following primary antibodies were used: CK8 (Throma-1; the University of Iowa, 1:50), Collagen I (SouthernBiotech 1310-01; 1:200), Collagen III (SouthernBiotech 1330-01; 1:200), Laminin 1 (Sigma L9393; 1:200), Tenascin C (Abcam ab108930; 1:200), αSMA (Sigma F3777; 1:200), FSP1 (a gift from Dr. Eric Neilson, Vanderbilt Univ.

Techniques: Recombinant, Electron Microscopy, Plasmid Preparation, SYBR Green Assay, Immunodetection, Bicinchoninic Acid Protein Assay, Modification, Luciferase, Derivative Assay, Isolation, shRNA, Control