Human/Mouse/Rat CTGF/CCN2 Antibody

Detection of Human, Mouse, and Rat CTGF/CCN2 by Western Blot.

Western blot shows lysates of HUVEC human umbilical vein endothelial cells, SVEC4-10 mouse vascular endothelial cell line, and Rat-2 rat embryonic fibroblast cell line. PVDF membrane was probed with 2 µg/mL of Rabbit Anti-Human/Mouse/Rat CTGF/CCN2 Monoclonal Antibody (Catalog # MAB91901) followed by HRP-conjugated Anti-Rabbit IgG Secondary Antibody (Catalog # HAF008). A specific band was detected for CTGF/CCN2 at approximately 36 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.

Detection of CTGF/CCN2 by Western Blot

The suppression of mitophagy inhibited cardiac fibroblasts (CF) activation. CF were transfected with either Pink1 siRNA or negative control (NC) and then stimulated with TGF-beta 1. (A) alpha-SMA immunofluorescence staining and semi-quantitative analysis. (B) Immunoblot analyses and quantitative analyses of the markers of CF activation, Postn and Ctgf, among the different groups. EdU and vimentin staining (C) and the MTS cell proliferation assay (D) were used to evaluate CF proliferation. (E) A wound healing assay was performed to evaluate CF migratory capacity following the different treatments. (F) Measurement of lysyl oxidase (LOX) activity. (G) The relative expression levels of extracellular matrix (ECM)-related proteins normalized to that of beta-actin. (H) Cell apoptosis was compared among the different groups by flow cytometry. Data are shown as mean ± standard error of the mean (n = 3 independent cell isolations per group). Means were compared by one-way ANOVA, followed by the Student–Newman–Keuls (SNK) post hoc test. *P < 0.05; **P < 0.01; ***P < 0.001. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/33585469), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of CTGF/CCN2 by Western Blot

Reducing the cardiac fibroblasts (CF) glycolytic flux may be important for mitochondrial fission inhibition-induced suppression of CF activation. (A) Measurements of the extracellular acidification rate (ECAR) metabolic profile by Seahorse XF glycolytic rate assay kit and analyses of CF Proton Efflux Rate (PER) in basal glycolysis and glycolysis capacity. (B) The oxygen consumption rate (OCR) as measured using a Seahorse XF Cell Mito Stress Test Kit and analyses of the OCR under basal and maximum respiration. (C) Western blot analyses and quantification of key glycolytic enzymes under TGF-beta 1 plus mdivi-1 cotreatment. (D) The expression of CF activation-related markers was measured by immunoblotting following TGF-beta 1 plus mdivi-1 cotreatment and in the presence or absence of 2-DG. Data are shown as mean ± standard error of the mean (n = 3 independent cell isolations per group). Means were compared by one-way ANOVA, followed by the Student–Newman–Keuls (SNK) post hoc test. ns, not significant; *P < 0.05; **P < 0.01; ***P < 0.001. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/33585469), licensed under a CC-BY license. Not internally tested by R&D Systems.