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. 2023 Jun 20;80(7):184. doi: 10.1007/s00018-023-04826-4

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — Inhibiting Dectin-1/Syk decreased the TGF-β1-signaling pathway. A RAW cells were treated with anti-Dectin-1 antibody (5 µg/mL) for 30 min, and then stimulated with Ang II (1 µM) for 24 h. Total proteins were extracted and subjected to analysis of TGF-β1 protein levels. GAPDH was used as loading control; B RAW cells were treated with anti-Dectin-1 antibody (5 µg/mL) for 30 min, and then stimulated with Ang II (1 µM) for 6 h. Real-time qPCR showing mRNA levels of tgfb1 of each group; C RAW cells were treated with anti-Dectin-1 antibody (5 µg/mL) for 30 min, and then stimulated with Ang II (1 µM) for 24 h. Representative images of TGF-β1 protein expression detected by immune fluorescence microscopy. The right panel shown the quantification of the average fluorescence as detected by immunofluorescence staining compared to Ctrl group. D RAW cells were treated with anti-Dectin-1 antibody (5 µg/mL) for 30 min, and then stimulated with Ang II (1 µM) for 24 h. TGF-β1 protein secretion were determined in the supernatants level of each group by an ELISA method; E RAW cells were treated with Syk inhibitor (R406, 10 µmol/mL) for 1 h, and then stimulated with Ang II (1 µM) for 24 h. Total proteins were extracted and subjected to analysis of TGF-β1 protein levels. GAPDH was used as loading control; F RAW cells were treated with Syk inhibitor (R406, 10 µmol/mL) for 1 h, and then stimulated with Ang II (1 µM) for 6 h. Real-time qPCR showing mRNA levels of tgfb1 of each group; G RAW cells were treated with Syk inhibitor (R406, 10 µmol/mL) for 1 h, and then stimulated with Ang II (1 µM) for 24 h. Representative images of TGF-β1 protein expression detected by immune fluorescence microscopy; H The quantification of the average fluorescence as detected by immunofluorescence staining compared to Ctrl group in Fig. 5G. I RAW cells were treated with Syk inhibitor (R406, 10 µmol/mL) for 1 h, and then stimulated with Ang II (1 µM) for 24 h. TGF-β1 protein secretion were determined in the supernatants level of each group by an ELISA method; J ChIP-qPCR analysis of blocking Dectin-1(D1Ab) and Syk antagonist (R406) inhibited the p65 binding to Tgfb1 promoter induced by Ang II in RAW cells, respectively. [A-J, n = 3; 1-way ANOVA followed by Tukey post-hoc tests (A-J: number of comparisons = 6; *P < 0.05, **P < 0.01, and ***P < 0.001]