mouse ctgf  (Elabscience Biotechnology)

Journal: Pharmaceutics

Article Title: Engineering Lipid Nanoparticles to Enhance Intracellular Delivery of Transforming Growth Factor-Beta siRNA (siTGF-β1) via Inhalation for Improving Pulmonary Fibrosis Post-Bleomycin Challenge.

doi: 10.3390/pharmaceutics17020157

Figure Lengend Snippet: Figure 5. Anti-fibrosis effect of siTGFβ1-LNPs in vitro. (A) Migration of HFL1 cells at different time points after different treatment (n = 3). (B) Measurement of ROS of Beas-2b cells after different treatment (n = 3). (C) HYP content measurement of Beas-2b cells supernatant after different treatment (n = 3). (D,E) ELISA analysis of the inflammation-related factor TGFβ1 and CTGF expression of Beas-2b cells supernatant after different treatment (n = 3). (F,G) qPCR analysis of the inflammation- related factor TGFβ1 and CTGF expression of Beas-2b cells supernatant after different treatment (n = 3). *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001.

Article Snippet: Then, the release levels of TGF-β1 and CTGF in cells were detected using TGF-β1 ELISA kit (Elabscience, Wuhan, China) and Mouse CTGF (Connective Tissue Growth Factor) ELISA kit (Elabscience, Wuhan, China), respectively.

Techniques: In Vitro, Migration, Enzyme-linked Immunosorbent Assay, Expressing

Journal: Pharmaceutics

Article Title: Engineering Lipid Nanoparticles to Enhance Intracellular Delivery of Transforming Growth Factor-Beta siRNA (siTGF-β1) via Inhalation for Improving Pulmonary Fibrosis Post-Bleomycin Challenge.

doi: 10.3390/pharmaceutics17020157

Figure Lengend Snippet: Figure 7. Inflammation-related factor TGFβ1 and CTGF expression and toxicity evaluation. (A–C) Im- munohistochemical staining for TGFβ1 and CTGF in different groups (n = 5), scale bar: 100 µm. (D,E) ELISA analysis of the inflammation-related factor TGFβ1 and CTGF expression in different groups (n = 5). (F,G) qPCR analysis of the inflammation-related factor TGFβ1 and CTGF expression in different groups (n = 5). (H) Histological H&E staining of major organs (heart, liver, spleen, lung, and kidney) scale bar: 100 µm. **, p < 0.01; ***, p < 0.001; ****, p < 0.0001.

Article Snippet: Then, the release levels of TGF-β1 and CTGF in cells were detected using TGF-β1 ELISA kit (Elabscience, Wuhan, China) and Mouse CTGF (Connective Tissue Growth Factor) ELISA kit (Elabscience, Wuhan, China), respectively.

Techniques: Expressing, Staining, Enzyme-linked Immunosorbent Assay

Journal: Cell Communication and Signaling : CCS

Article Title: The pathogenic role of succinate-SUCNR1: a critical function that induces renal fibrosis via M2 macrophage

doi: 10.1186/s12964-024-01481-5

Figure Lengend Snippet: Succinate stimulated macrophage infiltration, activation of profibrotic M2 phenotype, upregulation of profibrotic factors in vivo and in vitro. A F4/80 immunohistochemistry staining indicated succinate markedly increased renal macrophage in the kidney interstitium rather than glomerulus. *** P < 0.001, versus control group, n = 5. B Renal proinflammatory M1 cytokines, including iNOS and IL6 mRNA levels, were reduced by succinate. ** P < 0.01, versus the control group, n = 5. C The mRNA levels of anti-inflammatory M2 cytokines (Arg1, Fizz1, Mgl2, and IL-10) in the kidney were markedly increased. ** P < 0.01;*** P < 0.001, versus control group, n = 5. D Succinate upregulated renal M2 macrophages-related profibrotic factors expression (galectin3, MMP9, MMP12, MMP13, PDGF, and CTGF). ns, not significant; ** P < 0.01;*** P < 0.001, versus control group, n = 5. RAW 264.7 cells were treated at 500 μM succinate for 24 h, and quantitative PCR analysis and immunoblotting were adopted to detect the effects of succinate on M2 polarization and expression of profibrotic factors in vitro. E Succinate had no effects on the cell viability of RAW 264.7. Succinate downregulated M1 cytokines (iNOS and IL6) mRNA levels ( F ) while significantly upregulated M2 cytokines (Arg1, Fizz1, Mgl2, and IL-10) ( G ). *** P < 0.001, versus control group, n = 3, biologically repeated 3 times. Likewise, succinate remarkably increased M2 macrophage-related profibrotic factor expression (MMP9, MMP12, MMP13, PDGF, and CTGF) ( H ). ns, not significant; *** P < 0.001, versus control group, n = 3, biologically repeated 3 times. The cell supernatant was measured by mouse CTGF ELISA kit according to the manufacturer’s instructions (E-EL-M0340; Elabscience, Bethesda, MD). Similarly, succinate increased CTGF release of macrophages ( I )

Article Snippet: The cell supernatant was measured by mouse CTGF ELISA kit according to the manufacturer’s instructions (E-EL-M0340; Elabscience, Bethesda, MD).

Techniques: Activation Assay, In Vivo, In Vitro, Immunohistochemistry, Staining, Control, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: Cell Communication and Signaling : CCS

Article Title: The pathogenic role of succinate-SUCNR1: a critical function that induces renal fibrosis via M2 macrophage

doi: 10.1186/s12964-024-01481-5

Figure Lengend Snippet: CTGF neutralizing antibody inhibited the stimulation of fibroblasts by macrophage-conditioned medium. A CTGF antibody prevented the proliferative effects of CM on NRK-49F, indicated by the results of the CCK8 assay. *** P < 0.001, versus control group, n = 6 in CCK8, biologically repeated 3 times. B Also, the CTGF antibody suppressed the activation effects of CM on NRK-49F, as indicated by the results of the protein quantitative analysis of fibronectin and α-SMA. *** P < 0.001, versus control group, &&& P < 0.001, versus the succinate group, n = 3, biologically repeated 3 times

Article Snippet: The cell supernatant was measured by mouse CTGF ELISA kit according to the manufacturer’s instructions (E-EL-M0340; Elabscience, Bethesda, MD).

Techniques: CCK-8 Assay, Control, Activation Assay

Journal: Cell Communication and Signaling : CCS

Article Title: The pathogenic role of succinate-SUCNR1: a critical function that induces renal fibrosis via M2 macrophage

doi: 10.1186/s12964-024-01481-5

Figure Lengend Snippet: Succinate promoted CTGF expression through activation of β-catenin. A Succinate increased protein levels of non-p-β-catenin and β-catenin in the mice kidney. *** P < 0.001, versus control group, n = 5. RAW 264.7 was treated with 500 μM succinate for 12 h. B Succinate enhanced protein levels of non-p-β-catenin and β-catenin in the RAW 264.7. *** P < 0.001, versus control group, n = 3, biologically repeated 3 times. C Succinate promoted translocation of non-p-β-catenin into the nucleus. ICG-001 (2 μM) pretreatment RAW 264.7 for 1 h, 500 μM succinate stimulation for 24 h and 48 h. D ICG-001 prevented the increase of CTGF mRNA induced by succinate. *** P < 0.001, versus control group, &&& P < 0.001, versus the succinate group, n = 3, biologically repeated 3 times. E The elevation of CTGF protein level was also lowered by ICG-001. *** P < 0.001, versus control group, &&& P < 0.001, versus the succinate group, n = 3, biologically repeated 3 times

Article Snippet: The cell supernatant was measured by mouse CTGF ELISA kit according to the manufacturer’s instructions (E-EL-M0340; Elabscience, Bethesda, MD).

Techniques: Expressing, Activation Assay, Control, Translocation Assay

Journal: European journal of histochemistry : EJH

Article Title: Sodium hyaluronate promotes proliferation, autophagy, and migration of corneal epithelial cells by downregulating miR-18a in the course of corneal epithelial injury.

doi: 10.4081/ejh.2023.3663

Figure Lengend Snippet: Figure 1. SH markedly attenuated corneal epithelial tissue injury and upregulated CTGF in CEI model mice. A) Hematoxylin and eosin staining was used to observe pathological changes in the corneal epithelium of CEI model mice after treatment with SH. B,b) HIC was used to confirm the effect of SH on CTGF expression in mice with CEI. Magnification: B), x100; b) x200.

Article Snippet: The levels of CTGF and TGF-β were detected using CTGF ELISA kit (E-EL-M0340c; Elabscience, China) and TGF-β ELISA kit, respectively (E-EL-0162c; Elabscience), as described in the manufacturer’s instructions.

Techniques: Staining, Expressing

Journal: European journal of histochemistry : EJH

Article Title: Sodium hyaluronate promotes proliferation, autophagy, and migration of corneal epithelial cells by downregulating miR-18a in the course of corneal epithelial injury.

doi: 10.4081/ejh.2023.3663

Figure Lengend Snippet: Figure 2. SH markedly downregulated miR-18a expression and mediated autophagy-related protein expression in mice with CEI. CEI model mice were established and then treated with SH. A) Changes in miR-18a expression in mice were identified by using qPCR at 0, 12, 24, 48, and 72 h. B) RT-qPCR analyses of CTGF, TGF-β, Col1A1, and FN expression. C) The concentrations of CTGF and TGF-β were detected with ELISA kits at 72 h post injury. D,E) Western blotting was used to monitor changes in Col1A1, FN, LC3B, Beclin 1, and P62 expression in corneal tissues at 72 h post injury.

Article Snippet: The levels of CTGF and TGF-β were detected using CTGF ELISA kit (E-EL-M0340c; Elabscience, China) and TGF-β ELISA kit, respectively (E-EL-0162c; Elabscience), as described in the manufacturer’s instructions.

Techniques: Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Western Blot

Journal: European journal of histochemistry : EJH

Article Title: Sodium hyaluronate promotes proliferation, autophagy, and migration of corneal epithelial cells by downregulating miR-18a in the course of corneal epithelial injury.

doi: 10.4081/ejh.2023.3663

Figure Lengend Snippet: Figure 3. Overexpression of miR-18a attenuated the effects of SH on miR-18a, and autophagy-related pathways, CTGF and TGF-β level in CEI model mice. CEI model mice were treated with SH and injected with miR-18a mimics or an inhibitor, respectively. A) MiR-18a levels were determined by RT-qPCR. The levels of CTGF and TGF-β in each group were detected using RT-qPCR (B) and ELISA kits. C,D) Changes in LC3B, Beclin 1, and P62 expression were detected by Western blotting.

Article Snippet: The levels of CTGF and TGF-β were detected using CTGF ELISA kit (E-EL-M0340c; Elabscience, China) and TGF-β ELISA kit, respectively (E-EL-0162c; Elabscience), as described in the manufacturer’s instructions.

Techniques: Over Expression, Injection, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Expressing, Western Blot

Journal: European journal of histochemistry : EJH

Article Title: Sodium hyaluronate promotes proliferation, autophagy, and migration of corneal epithelial cells by downregulating miR-18a in the course of corneal epithelial injury.

doi: 10.4081/ejh.2023.3663

Figure Lengend Snippet: Figure 4. Treatment with miR-18a dramatically reversed the induction effect of SH on the cell viability, CTGF and TGF-β of CEI model cells. CEI cell model was constructed using HCECs that were exposed to UV radiation. Next, the HCECs were treated with SH and miR-18a mimics. A) RT-qPCR analysis of miR-18a. B) CCK8 assays were performed to assess changes in cell viability. C) ELISA kits were used to detect the concentrations of CTGF and TGF-β. D) Edu assays revealed changes in cell proliferation. Magnification: x100.

Article Snippet: The levels of CTGF and TGF-β were detected using CTGF ELISA kit (E-EL-M0340c; Elabscience, China) and TGF-β ELISA kit, respectively (E-EL-0162c; Elabscience), as described in the manufacturer’s instructions.

Techniques: Construct, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay