Journal: Oncotarget

Article Title: Epithelial derived CTGF promotes breast tumor progression via inducing EMT and collagen I fibers deposition

doi:

Figure Lengend Snippet: Kaplan–Meier curves showing the overall survival and recurrence-free survival of patients with low or high tumor epithelial or stroma CTGF expression in the combined cohort of 103 breast cancer patients, P values were determined by log rank test.

Article Snippet: Overexpression of full-length CTGF gene was achieved by transfection of cDNA for CTGF (OriGene Technologies), which clones the open reading frame (ORF) of this gene into the pCMV6 Entry vector.

Techniques: Expressing

Journal: Oncotarget

Article Title: Epithelial derived CTGF promotes breast tumor progression via inducing EMT and collagen I fibers deposition

doi:

Figure Lengend Snippet: A–B. Quantitative graphs and representative CTGF immunohistochemistry staining of the breast tumor PDX tissue microarray. H score was calculated as described in Methods. P values were determined by student t -test. C. Representative images showing the Masson's trichrome staining and CTGF immunohistochemistry staining of the triple-negative (TNBC) and HER2-positive (HRE2+) breast tumor PDX tissue microarray. D. Correlation between the H scores of CTGF in tumor cells and % of stroma area in the TNBC tissue microarrays. R 2 = 0.66. E. Correlation between the H scores of CTGF in stromal cells and % of stroma area in the TNBC tissue microarrays. R 2 = 0.39. F. Correlation between the H scores of CTGF in stromal cells and % of stroma area in the HER2+ tissue microarrays. R 2 = 0.43.

Article Snippet: Overexpression of full-length CTGF gene was achieved by transfection of cDNA for CTGF (OriGene Technologies), which clones the open reading frame (ORF) of this gene into the pCMV6 Entry vector.

Techniques: Immunohistochemistry, Staining, Microarray

Journal: Oncotarget

Article Title: Epithelial derived CTGF promotes breast tumor progression via inducing EMT and collagen I fibers deposition

doi:

Figure Lengend Snippet: A–B. The co-expression analysis between CTGF and FN1, VIM, CDH1 in the n = 22 clinical breast tumor cohort . All gene probes were listed for FN1, VIM and CDH1 . The correlation co-efficient (cc) were calculated based on the log2 median-centered intensity of FN1, VIM, CDH1 and CTGF. C–D. The co-expression analysis between CTGF and FN1, VIM, CDH1 in the n = 66 clinical breast tumor cohort . E–H. CTGF gene expression in a series EMT-induced human mammary epithelial cell (HMLER) cell lines, including over-expression of EMT transcription factor Goosecoid (GSC), Snail, or Twist, and induction of EMT by TGFB1 transfection. P values were determined by student t -test. Fold change was log 2 scale.

Article Snippet: Overexpression of full-length CTGF gene was achieved by transfection of cDNA for CTGF (OriGene Technologies), which clones the open reading frame (ORF) of this gene into the pCMV6 Entry vector.

Techniques: Expressing, Gene Expression, Over Expression, Transfection

Journal: Oncotarget

Article Title: Epithelial derived CTGF promotes breast tumor progression via inducing EMT and collagen I fibers deposition

doi:

Figure Lengend Snippet: A. Representative phase-contrast images showing the elongated morphology of over-CTGF-HMLER cells which is typically associated with mesenchymal phenotype. B. RT-PCR analysis of the EMT genes and CTGF in the control and over-CTGF-HMLER cells. Relative gene expression level to GAPDH was plotted. C. Western blot analysis of the EMT markers and CTGF in the control and over-CTGF-HMLER cells. D–E. Quantitative graphs and representative membrane images showing the migration ability of the control and over-CTGF-HMLER cells measured by the Boyden Chamber assay. F. Quantitative graphs showing the invasion ability of the control and over-CTGF-HMLER cells measured by coating Matrigel in the Boyden Chamber assay. G–H. Enforced expression of CTGF in the HMLER cells promoted the number and size of mammospheres. I. Western blot analysis of enriched CD44 expression in the mammospheres. ** P < 0.01, vs control. P values were determined by student t -test.

Article Snippet: Overexpression of full-length CTGF gene was achieved by transfection of cDNA for CTGF (OriGene Technologies), which clones the open reading frame (ORF) of this gene into the pCMV6 Entry vector.

Techniques: Reverse Transcription Polymerase Chain Reaction, Control, Gene Expression, Western Blot, Membrane, Migration, Boyden Chamber Assay, Expressing

Journal: Oncotarget

Article Title: Epithelial derived CTGF promotes breast tumor progression via inducing EMT and collagen I fibers deposition

doi:

Figure Lengend Snippet: A. Representative phase-contrast images showing the epithelial morphology of the shCTGFs knockdown cells. B. Western blot analysis of the CTGF and N-cadherin, E-cadherin in the control and shCTGFs cells. C–D. Quantitative graphs and representative membrane images showing the migration ability of the control and shCTGFs cells measured by the Boyden Chamber assay. E. Quantitative graphs showing the invasion ability of the control and shCTGFs cells measured by coating Matrigel in the Boyden Chamber assay. F–G. CTGF depletion in the HMLER-snail cells reduced the number and size of mammospheres. H. Western blot analysis of CD44 in the mammospheres. * P < 0.05, vs control; ** P < 0.01, vs control. P values were determined by student t -test.

Article Snippet: Overexpression of full-length CTGF gene was achieved by transfection of cDNA for CTGF (OriGene Technologies), which clones the open reading frame (ORF) of this gene into the pCMV6 Entry vector.

Techniques: Knockdown, Western Blot, Control, Membrane, Migration, Boyden Chamber Assay

Journal: Oncotarget

Article Title: Epithelial derived CTGF promotes breast tumor progression via inducing EMT and collagen I fibers deposition

doi:

Figure Lengend Snippet: A–B. In vivo tumor growth of the over-CTGF-HMLER cells and control HMLER cells mixed with Matrigel (A) and PBS (B) C. Representative images showing the Masson's trichrome staining of the tumor connective tissue, and second harmonic generation (SHG) imaging of the intra-tumoral collagen I fibers, of the Matrigel-mixed over-CTGF-HMLER tumors. D–E. In vivo tumor growth of the shCTGF-HMLER cells (D), and representative Masson's trichrome staining and SHG imaging of the intra-tumoral collagen I fibers. F. Quantification of the percentage of collagen fiber and perpendicular collagen fiber to the overall connective tissue area. Mouse tumor sections (10 μm thick) were cut serially, and one section from every 100 μm was stained by Masson's trichrome staining, and the adjacent section was imaged by SHG imaging. In each section 5–10 fields were quantified. N = 4 mouse tumors in each group. * P < 0.05, vs control HMLER; ^ P < 0.05, vs HMLER-snail. P values were determined by student t -test.

Article Snippet: Overexpression of full-length CTGF gene was achieved by transfection of cDNA for CTGF (OriGene Technologies), which clones the open reading frame (ORF) of this gene into the pCMV6 Entry vector.

Techniques: In Vivo, Control, Staining, Imaging

Journal: Oncotarget

Article Title: Epithelial derived CTGF promotes breast tumor progression via inducing EMT and collagen I fibers deposition

doi:

Figure Lengend Snippet: A–B. A precedent treatment with anti-TNFR1 monoclonal antibody (10 μg/ml) more profoundly prevented the increase of CTGF-induced TNFR1 expression in the CTGF-highly expressed cells (over-CTGF-HMLER and HMLER-snail) than that in the CTGF-lowly expressed cells (control-HMLER and shCTGF2). C. Representative phase-contrast images showing the cell morphology changes in the indicated cell lines and treatments. D–E. The activation of IKBKA and IKBKB by CTGF could be specifically attenuated by the anti-TNFR1 antibody in the CTGF-high tumor cells. F. JUK but not ERK1/2 and p38 in the MAPK signaling pathway was up-regulated by exogenous CTGF in the CTGF-low tumor cells. G. Knockdown CTGF in the HMLER-snail cells down-regulated the IKBKA and IKBKB, and such down-regulation could be rescued by exogenous CTGF. All experimental data are representative of at least two independent experiments performed in triplicate. Data are expressed as mean ± s.e.m.

Article Snippet: Overexpression of full-length CTGF gene was achieved by transfection of cDNA for CTGF (OriGene Technologies), which clones the open reading frame (ORF) of this gene into the pCMV6 Entry vector.

Techniques: Expressing, Control, Activation Assay, Knockdown

Journal: Oncotarget

Article Title: Epithelial derived CTGF promotes breast tumor progression via inducing EMT and collagen I fibers deposition

doi:

Figure Lengend Snippet: A–B. Cell proliferation and mammosphere formation were significantly inhibited by the anti-TNFR1 treatment in over-CTGF-HMLER and HMLE-snail cells but not control-HMLER cells or shCTGF-HMLE-snail. C–D. Cell proliferation and mammosphere formation were significantly inhibited by resveratrol treatment in over-CTGF-HMLER and HMLE-snail cells but not control-HMLER cells or shCTGF-HMLE-snail. * P < 0.05, ** P < 0.01, vs anti-TNFR1(−) or resveratrol (−) group of the corresponding cell lines. P values were determined by student t -test.

Article Snippet: Overexpression of full-length CTGF gene was achieved by transfection of cDNA for CTGF (OriGene Technologies), which clones the open reading frame (ORF) of this gene into the pCMV6 Entry vector.

Techniques: Control

Journal: Oncotarget

Article Title: Epithelial derived CTGF promotes breast tumor progression via inducing EMT and collagen I fibers deposition

doi:

Figure Lengend Snippet: CTGF is mainly derived from epithelial tumor cells. Through the CTGF-TNFR1-IκB autocrine signaling, CTGF promotes tumor EMT which contributes to the stemness and metastasis. Through promoting the deposition and orientation of collagen I fibers in the primary tumor stroma, CTGF promotes stroma-tumor interaction which facilitates tumor progression.

Article Snippet: Overexpression of full-length CTGF gene was achieved by transfection of cDNA for CTGF (OriGene Technologies), which clones the open reading frame (ORF) of this gene into the pCMV6 Entry vector.

Techniques: Derivative Assay

Journal: Acta Pharmaceutica Sinica. B

Article Title: AI-powered therapeutic aptamer drug discovery: Targeting the CT-domain of CTGF for duchenne muscular dystrophy

doi: 10.1016/j.apsb.2026.02.016

Figure Lengend Snippet: CT-domain is an optimal domain without elevating compensatory TGF- β 1 level rather than VWC-domain. (a) The levels of supernatant fibrosis markers (fibronectin and collagen III) in CTGF ko (CTGF knock out) fibroblast expressing full-length CTGF (FL-CTGF), CTGF with VWC-domain deficiency (CTGF-ΔVWC), and CTGF with CT-domain deficiency (CTGF-ΔCT), respectively (upper). Statistical analysis of ratios of fibronectin and collagen III to GAPDH (lower). (b) The levels of supernatant TGF- β 1 in CTGF ko fibroblast expressing FL-CTGF, CTGF-ΔVWC and CTGF-ΔCT, respectively (upper). Statistical analysis of ratios of TGF- β 1 to GAPDH (lower). (c) The ELISA analysis of TGF- β 1 levels in fibroblast treated with CTGF (1.5 μg/mL), CTGF + FG-3019 (0.01 μg/mL), CTGF + IgG (0.05 μg/mL), CTGF + FG-3019 (0.1 μg/mL), CTGF + IgG (0.01 μg/mL), CTGF + FG-3019 (0.05 μg/mL), CTGF + IgG (0.1 μg/mL) for 48 h, respectively. (d) The Western blot analysis of fibronectin and collagen III levels in fibroblast treated with CTGF, CTGF + FG-3019, CTGF + TGF- β 1 antibody (CTGF + TGF- β 1 ab), CTGF + FG-3019 + TGF- β 1 antibody (CTGF + F + T), and CTGF + IgG for 48 h, respectively (left). Statistical analysis of ratios of fibronectin and collagen III levels to GAPDH, respectively (right). (e) The Western blot analysis of fibronectin and collagen III levels in diagram muscle of WT mice treated with PBS, Mdx mice treated with PBS, FG-3019, TGF- β 1 antibody (TGF- β 1 ab), FG-3019 + TGF- β 1 antibody (CTGF + F + T), and IgG for 6 weeks, respectively (left). Statistical analysis of ratios of fibronectin and collagen III levels to GAPDH, respectively (right). Data are expressed as mean ± SD followed by one-way ANOVA with Tukey’s post hoc test, n = 3 per group. ∗ P < 0.05. ∗∗ P < 0.01. ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

Article Snippet: Mice were randomly assigned to one of four experimental groups: (1) Vehicle Control Group: Received subcutaneous (s.c.) injections of the formulation buffer alone ( e.g., PBS or vehicle used for Apc003OA), once weekly for 12 weeks. (2) Apc003OA Treatment Group: Received s.c. injections of Apc003OA at a dose of 100 mg/kg body weight, dissolved in the appropriate vehicle, once weekly for 12 weeks. (3) FG-3019 Treatment Group: Received s.c. injections of the CTGF VWC-domain specific antibody FG-3019 (purchased from Med Chem Express) administered according to an equivalent schedule and dose regimen as a comparator. (4) Apc003OA + BP Pre-treatment Group: Received an s.c. injection of the blocking peptide (BP) designed against the CT-domain of CTGF binding site for Apc003 ( e.g ., at a dose and timepoint defined in pilot studies, such as 1 h prior to each Apc003OA dose), followed by s.c. injection of Apc003OA (100 mg/kg), once weekly for 12 weeks.

Techniques: Knock-Out, Expressing, Enzyme-linked Immunosorbent Assay, Western Blot

Journal: Acta Pharmaceutica Sinica. B

Article Title: AI-powered therapeutic aptamer drug discovery: Targeting the CT-domain of CTGF for duchenne muscular dystrophy

doi: 10.1016/j.apsb.2026.02.016

Figure Lengend Snippet: Apc003OA could distribute and remain in muscle tissues for an extended period, whereas FG-3019 could not do so. (a) The in vivo distribution of Cy3-Apc003OA and Cy3-FG-3019 in muscles (diaphragm and gastrocnemius) and major organs (heart, liver, spleen, lung, and kidney) 2, 4, 12 and 24 h after subcutaneous injection, respectively. (b) Fluorescence intensities of Cy3-Apc003OA and Cy3-FG-3019 in muscles and major organs 2, 4, 12 and 24 h after subcutaneous injection, respectively. Data are expressed as mean ± standard deviation followed by multiple unpaired t tests, n = 3 per group. ∗ P < 0.05. ∗∗ P < 0.01. ∗∗∗ P < 0.001. ∗∗∗∗ P < 0.0001. The P values for the respective comparisons are indicated on the graph. Note: The data were presented as the means ± standard deviation.

Article Snippet: Mice were randomly assigned to one of four experimental groups: (1) Vehicle Control Group: Received subcutaneous (s.c.) injections of the formulation buffer alone ( e.g., PBS or vehicle used for Apc003OA), once weekly for 12 weeks. (2) Apc003OA Treatment Group: Received s.c. injections of Apc003OA at a dose of 100 mg/kg body weight, dissolved in the appropriate vehicle, once weekly for 12 weeks. (3) FG-3019 Treatment Group: Received s.c. injections of the CTGF VWC-domain specific antibody FG-3019 (purchased from Med Chem Express) administered according to an equivalent schedule and dose regimen as a comparator. (4) Apc003OA + BP Pre-treatment Group: Received an s.c. injection of the blocking peptide (BP) designed against the CT-domain of CTGF binding site for Apc003 ( e.g ., at a dose and timepoint defined in pilot studies, such as 1 h prior to each Apc003OA dose), followed by s.c. injection of Apc003OA (100 mg/kg), once weekly for 12 weeks.

Techniques: In Vivo, Muscles, Injection, Fluorescence, Standard Deviation

Journal: Acta Pharmaceutica Sinica. B

Article Title: AI-powered therapeutic aptamer drug discovery: Targeting the CT-domain of CTGF for duchenne muscular dystrophy

doi: 10.1016/j.apsb.2026.02.016

Figure Lengend Snippet: Apc003OA exerted better fibrosis inhibitory activity without elevating compensatory TGF- β 1 levels than FG-3019 in mdx mice. (a) The specific force against stimulation frequency of soleus muscles in WT mice treated with PBS, and mdx mice treated with PBS, Apc003OA, FG-3019, Apc003OA + BP, and BP for 12 weeks, respectively. (b) The forelimb grip strengths of mdx mice treated with PBS, and mdx mice treated with PBS, Apc003OA, FG-3019, Apc003OA + BP and BP for 12 weeks, respectively. (c) The fibronectin and collagen III levels in diaphragm muscle of WT mice treated with PBS, mdx mice treated with PBS, Apc003OA, FG-3019, Apc003OA + BP and BP for 12 weeks, respectively (left). Statistical analysis of fibronectin and collagen III intensity ratios to GAPDH (right). (d) The diaphragm muscle using Masson's staining from WT mice treated with PBS, and mdx mice treated with PBS, Apc003OA, FG-3019, Apc003OA + BP, and BP for 12 weeks, respectively (left). The statistical analysis of fibrosis index (right). (e) The serum levels of TGF- β 1 in WT mice treated with PBS, and mdx mice treated with PBS, Apc003OA, FG-3019, Apc003OA + BP and BP for 12 weeks, respectively. Data are expressed as mean ± standard deviation followed by one-way ANOVA with Tukey’s post hoc test, n = 5 per group. ∗ P < 0.05. ∗∗ P < 0.01. ∗∗∗ P < 0.001. ∗∗∗∗ P < 0.0001. The P values for the respective comparisons are indicated on the graph. Note: BP: Blocking peptide. WT: wild type (C57BL/10ScSn mice). Administration route: subcutaneous injection. Dosing frequency: once a week.

Article Snippet: Mice were randomly assigned to one of four experimental groups: (1) Vehicle Control Group: Received subcutaneous (s.c.) injections of the formulation buffer alone ( e.g., PBS or vehicle used for Apc003OA), once weekly for 12 weeks. (2) Apc003OA Treatment Group: Received s.c. injections of Apc003OA at a dose of 100 mg/kg body weight, dissolved in the appropriate vehicle, once weekly for 12 weeks. (3) FG-3019 Treatment Group: Received s.c. injections of the CTGF VWC-domain specific antibody FG-3019 (purchased from Med Chem Express) administered according to an equivalent schedule and dose regimen as a comparator. (4) Apc003OA + BP Pre-treatment Group: Received an s.c. injection of the blocking peptide (BP) designed against the CT-domain of CTGF binding site for Apc003 ( e.g ., at a dose and timepoint defined in pilot studies, such as 1 h prior to each Apc003OA dose), followed by s.c. injection of Apc003OA (100 mg/kg), once weekly for 12 weeks.

Techniques: Activity Assay, Muscles, Staining, Standard Deviation, Blocking Assay, Injection

Journal: Cancer Cell International

Article Title: MiR-218 regulates epithelial–mesenchymal transition and angiogenesis in colorectal cancer via targeting CTGF

doi: 10.1186/s12935-018-0575-2

Figure Lengend Snippet: CTGF was a direct target of miR-218 and could restore its inhibition effects on CRC progression. a , b miR-218 was able to suppress the mRNA ( a ) and protein ( b ) expression of CTGF. c , d miR-218 could inhibit the luciferase reported activity to 50%, demonstrating that it directly targeted CTGF. e CTGF treatment rescued the inhibition effects on EMT associated proteins brought by miR-218 over expression. f CTGF treatment restored the inhibition effects on VEGFA and ANGPT2 brought by miR-218 over expression. N = 3, **P < 0.01, t-test

Article Snippet: Recombinant Human CTGF Protein was purchased from R&D systems (9190-CC-050, USA) and added to culture medium at a final concentration of 10 ng/mL for 30 min before indicated experiments.

Techniques: Inhibition, Expressing, Luciferase, Activity Assay, Over Expression

Journal: Nature Communications

Article Title: Switch-like enhancement of epithelial-mesenchymal transition by YAP through feedback regulation of WT1 and Rho-family GTPases

doi: 10.1038/s41467-019-10729-5

Figure Lengend Snippet: YAP regulates E-cadherin through WT1 in epithelial layers on NRA. a Immunofluorescence staining for WT1 in YAP KD cell sheets (top), and for YAP in WT1 KD cell sheets cultured on NRA. The samples were fixed after 8 h to remove stencils. b Co-IP analysis using the YAP antibody, followed by immunoblotting using the WT1 antibody. c Chromatin immunoprecipitation (ChIP) analysis of the WT1-YAP complex binding at the E-cadherin promoter ( n = 3). We extracted cross-linked chromatin and immunoprecipitated it using antibodies against YAP, WT1, IgG (negative control), and RNAPII or histone H3 (see Supplementary Fig. ) antibodies (positive controls). The immunoprecipitated chromatin and input genomic DNA were used for amplification of the E-cadherin promoter, CTGF promoter (known to be regulated by YAP but not WT1, and used as another control), and GAPDH promoter ( n = 4 biologically independent samples, * = statistical significance of PCR products from each sample vs. IgG, * P < 0.05 and ** P < 0.01). d E-cadherin expressions of control and WT1 KD cells analyzed by immunoblotting with WT1 and E-cadherin antibodies ( n = 3 biologically independent samples, * = statistical significance of E-cadherin expression of control and WT1 KD cells, *** P < 5 × 10 −3 ). e Cell migration speed of individual cells in control and WT1 KD epithelial cells in the marginal region of the sheets in the presence of an E-cadherin blocking antibody (each number of independently analyzed cells, n , is indicated, * = statistical significance, n.s = no significance, and *** P < 5 × 10 −3 ). f Dissemination of cells in control and WT1 KD epithelial sheets on NRA in the presence of an E-cadherin blocking antibody ( n = 4 biologically independent experiments, * = statistical significance, * P < 0.05, *** P < 5 × 10 −3 , and n.s = no significance). g Immunoblotting of phosphorylated YAP and total YAP in cell sheets cultured in the presence of different concentrations of E-cadherin blocking antibody ( n = 3 biologically independent samples). h Schematic of the YAP-mediated cell dissemination triggered by mechanical cues stemming from NRA, operating through E-cadherin control by YAP-WT1 complexes and leading to cell dissemination in epithelial cell sheets on NRA. All error bars are S.E.M and statistical significance was determined by two-sided Student’s t -test

Article Snippet: Also, we used SimpleChIP® Human CTGF promoter primers (Cell Signaling, 14927) and GAPDH promoter primer in the kit (Thermo Fisher Scientific, 26516) as control primers.

Techniques: Immunofluorescence, Staining, Cell Culture, Co-Immunoprecipitation Assay, Western Blot, Chromatin Immunoprecipitation, Binding Assay, Immunoprecipitation, Negative Control, Amplification, Control, Expressing, Migration, Blocking Assay

Journal: Revista da Sociedade Brasileira de Medicina Tropical

Article Title: Role of transforming growth factor-beta 1 and connective tissue growth factor levels in coronavirus disease-2019-related lung Injury: a prospective, observational, cohort study

doi: 10.1590/0037-8682-0615-2021

Figure Lengend Snippet: Study groups’ TGF-β1, CTGF, and other laboratory parameter results

Article Snippet: TGF-β1 and CTGF values were determined using the ELISA method with a Human TGF-β1 ELISA kit (Elabscience, Human TGF-β1: cat. E-EL-H0110, Texas, USA) and a human CTGF ELISA kit (Elabscience, Human CTGF: E-EL-H0828, Texas, USA) in accordance with the manufacturer’s recommendations.

Techniques:

Journal: Revista da Sociedade Brasileira de Medicina Tropical

Article Title: Role of transforming growth factor-beta 1 and connective tissue growth factor levels in coronavirus disease-2019-related lung Injury: a prospective, observational, cohort study

doi: 10.1590/0037-8682-0615-2021

Figure Lengend Snippet: Box-plot presentation of serum TGF-β1 and CTGF levels on day 7 of admission in Group 1 divided by severity of COVID-19 disease. *:p<0.001 (analysis of variance) two-way comparison of subgroups.

Article Snippet: TGF-β1 and CTGF values were determined using the ELISA method with a Human TGF-β1 ELISA kit (Elabscience, Human TGF-β1: cat. E-EL-H0110, Texas, USA) and a human CTGF ELISA kit (Elabscience, Human CTGF: E-EL-H0828, Texas, USA) in accordance with the manufacturer’s recommendations.

Techniques: Comparison

Journal: Revista da Sociedade Brasileira de Medicina Tropical

Article Title: Role of transforming growth factor-beta 1 and connective tissue growth factor levels in coronavirus disease-2019-related lung Injury: a prospective, observational, cohort study

doi: 10.1590/0037-8682-0615-2021

Figure Lengend Snippet: Changes in serum TGF-β1 and CTGF levels among disease severity subgroups.

Article Snippet: TGF-β1 and CTGF values were determined using the ELISA method with a Human TGF-β1 ELISA kit (Elabscience, Human TGF-β1: cat. E-EL-H0110, Texas, USA) and a human CTGF ELISA kit (Elabscience, Human CTGF: E-EL-H0828, Texas, USA) in accordance with the manufacturer’s recommendations.

Techniques:

Journal: Revista da Sociedade Brasileira de Medicina Tropical

Article Title: Role of transforming growth factor-beta 1 and connective tissue growth factor levels in coronavirus disease-2019-related lung Injury: a prospective, observational, cohort study

doi: 10.1590/0037-8682-0615-2021

Figure Lengend Snippet: Determination of the diagnostic sensitivity and specificity of serum TGF-β1 and CTGF levels on days 1 and 7 of admission in patients diagnosed with COVID-19 using ROC curve analysis. ROC: receiver-operating characteristic curve.

Article Snippet: TGF-β1 and CTGF values were determined using the ELISA method with a Human TGF-β1 ELISA kit (Elabscience, Human TGF-β1: cat. E-EL-H0110, Texas, USA) and a human CTGF ELISA kit (Elabscience, Human CTGF: E-EL-H0828, Texas, USA) in accordance with the manufacturer’s recommendations.

Techniques: Diagnostic Assay

Journal: The Journal of endocrinology

Article Title: Intrinsic biological activity of the thrombospondin structural homology repeat in connective tissue growth factor.

doi: 10.1677/joe.1.06719

Figure Lengend Snippet: Figure 3 Stimulation of p44/p42 MAPK phosphorylation by CCN23. (A) 5·0105 HSC/well were cultured in 6-well plates until they were 80–90% confluent, after which the medium was replaced with serum-free DMEM for 48 h. The cells were then treated with TGF-1, CCN2, or CCN23 at the indicated doses for 30 min. Cells were harvested, lysed and subjected to Western blot with anti-p42/p44 or anti-phospho-p42/p44 antibodies. (B) Time course of p42/p44 MAPK phosphorylation following stimulation of serum-starved HSC with 50 ng/ml CCN23. (C) Serum-starved HSC were pretreated with 0–10 M PP2 for one hour and then stimulated with 50 ng/ml CCN23 for 30 min prior to Western blot detection of activated or total p42/p44 MAPK. The results are representative of three independent experiments.

Article Snippet: Controls included 50 ng/ml full-length human recombinant CCN2 (Ball et al. 2003b) or 2 ng/ml transforming growth factor beta 1(TGF- 1; R&D Systems, Minneapolis, MN, USA).

Techniques: Phospho-proteomics, Cell Culture, Western Blot

Journal: The Journal of endocrinology

Article Title: Intrinsic biological activity of the thrombospondin structural homology repeat in connective tissue growth factor.

doi: 10.1677/joe.1.06719

Figure Lengend Snippet: Figure 4 Promotion of pro-fibrogenic pathways in HSC by CCN23. 2·510 5 HSC/well were cultured in 6-well plates until they were 80–90% confluent, after which the medium was replaced with serum-free DMEM for 48 h. The cells were treated with TGF-1 (2 ng/ml), full-length CCN2 (50 ng/ml) or CCN23 (50, 100 ng/ml) in serum-free medium for 48 h at the indicated concentrations and then extracted for protein or RNA analysis by RT-PCR or Western blot, respectively. (A) FN mRNA (upper panel), -actin mRNA (middle panel) or FN protein (lower panel) and (B) Pro-collagen type IV(5) mRNA (upper panel) and -actin mRNA (lower panel).

Article Snippet: Controls included 50 ng/ml full-length human recombinant CCN2 (Ball et al. 2003b) or 2 ng/ml transforming growth factor beta 1(TGF- 1; R&D Systems, Minneapolis, MN, USA).

Techniques: Cell Culture, Reverse Transcription Polymerase Chain Reaction, Western Blot