Journal: Materials Today Bio

Article Title: Uniform and controllable surface nano-structure on polyetheretherketone implants can regulate mechanical property to enhance soft tissue integration through Piezo1/TGF-β1 signaling axis

doi: 10.1016/j.mtbio.2025.101645

Figure Lengend Snippet: The impact of nanoscale modification of PEEK implant surfaces on the mechanical perception, proliferation, and expression of fibrosis-related proteins in L929 cells. (A) The expression levels of mechanical perception, proliferation, and fibrosis-related proteins were evaluated in L929 cells cultured on different nanoscale modified PEEK surfaces at multiple time points. (B) The secretion of TGF-β1 from L929 cells cultured on various nanoparticle-modified PEEK surfaces was quantified using Elisa at multiple time points. (C) Immunofluorescence analysis was conducted to assess the expression differences of Piezo1, ITGB1, and α-SMA in L929 cells cultured on different nanoparticle-modified PEEK surfaces. (D) Quantitative fluorescence analysis was performed on the data presented in C.

Article Snippet: TGF-β1 Mouse/Rat (HEK293) (HY-P70648, MedChemExpress LLC., USA).

Techniques: Modification, Expressing, Cell Culture, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Fluorescence

Journal: Materials Today Bio

Article Title: Uniform and controllable surface nano-structure on polyetheretherketone implants can regulate mechanical property to enhance soft tissue integration through Piezo1/TGF-β1 signaling axis

doi: 10.1016/j.mtbio.2025.101645

Figure Lengend Snippet: Piezo1 mediates the proliferation and fibrosis enhancement of L929 cells on PEEK implants modified with a 500 nm surface treatment. (A) Changes in calcium influx induced by the specific Piezo1 agonist (Yoda1) and the calcium channel inhibitor (GsMTx-4) were assessed using Fluo-4AM. (B) The fluorescence intensity of calcium accumulation in L929 cells following treatment with Yoda1 and GsMTx-4 was observed under a fluorescence microscope. (C) Quantitative analysis of the average fluorescence intensity presented in B. (D) The regulatory effects of Piezo1 on proliferation-related pathways, fibrosis processes, and adhesion-associated proteins were evaluated separately on PEEK and PEEK-500. (E) RT-qPCR was employed to assess the transcriptional differences in fibrosis-related genes in L929 cells following the activation or inhibition of Piezo1. (F) Changes in TGF-β1 secretion by L929 cells after the activation or inhibition of Piezo1 were analyzed. (G) The involvement of TGF-β1 in fibrosis regulation through the activation and upregulation of Piezo1 was confirmed. (H) Schematic representation of the mechanism by which L929 cells detect mechanical signals from PEEK samples to facilitate soft tissue integration.

Article Snippet: TGF-β1 Mouse/Rat (HEK293) (HY-P70648, MedChemExpress LLC., USA).

Techniques: Modification, Fluorescence, Microscopy, Quantitative RT-PCR, Activation Assay, Inhibition

Journal: Food Science & Nutrition

Article Title: Dihydroquercetin Attenuates Silica‐Induced Pulmonary Fibrosis by Modulating the Gut Microbiota and the Serum Metabolites in Mice

doi: 10.1002/fsn3.71389

Figure Lengend Snippet: DHQ treatment attenuated silica‐induced pulmonary fibrosis in C57/BL6 mice. (A, B) DHQ treatment increased the body weight and decreased pulmonary index in silicosis model mice. The changes of body weight (C) The levels of pro‐inflammatory cytokines (IL‐1β, TNF‐α, and TGF‐β) in serum from different groups at day 21 were detected by ELISA assay. (D) Representative pictures (×200) of HE‐stained and Masson‐stained lung sections from mice on day 21 were shown. Bar = 100 μm. (E, F) The inflammation and fibrosis score numbers of 0–3, corresponding to the grades of –, +, ++, and +++, were evaluated by experienced pathologists in a blinded fashion. (G) Representative results of western blot for α‐SMA, collagen I and fibronectin in lung tissues and the quantification of results. Data are shown as mean ± SD. All experiments were repeated three times. # p < 0.05, ## p < 0.01 vs. the control group; * p < 0.05, ** p < 0.01 vs. the SiO 2 group.

Article Snippet: Sigma‐Aldrich provided the SiO 2 (Cat#S5631) particles (around 80% diameter 1‐5 μm), which were filtered through sedimentation following Stokes' law, underwent acidic hydrolysis, and were baked overnight at 200°C for 16 h. Interleukin‐1β (IL‐1β) (CSB‐E08054m), tumor necrosis factor‐α (TNF‐α) (CSB‐E04741m), and transforming growth factor‐β (TGF‐β) (CSB‐E04726m) were acquired from Cusabio Biotechnology in Wuhan, China.

Techniques: Enzyme-linked Immunosorbent Assay, Staining, Western Blot, Control

Journal: The Journal of Immunology Author Choice

Article Title: IDO1 and TGF-β Mediate Protective Effects of IFN-α in Antigen-Induced Arthritis

doi: 10.4049/jimmunol.1502125

Figure Lengend Snippet: The protective effect of IFN-α against AIA is mediated by TGF-β signaling in the sensitization phase. (A) Schematic representation of the AIA model, as described in Materials and Methods. Briefly, AIA was induced in WT Sv129 mice and LysM Cre+/−Tgfbr2fl/fl with or without IFN-α treatment. TGF-β signaling was blocked in WT mice by daily i.p. injection of 150 μg anti–TGF-β Ab for the first 0–8 or 20–28 d of AIA. (B) The level of arthritis is expressed as severity score (mean ± SEM, n ≥ 4) from WT mice with or without IFN-α and anti–TGF-β treatment. (C) Representative histochemical slides showing inflammation of the knee joint from each group. (D) Level of arthritis expressed as severity score (mean ± SEM, n ≥ 6) from LysM Cre+/−Tgfbr2fl/fl mice with or without IFN-α treatment. Comparison of arthritis severity score between different treatment groups was done by Mann–Whitney U test (*p < 0.05).

Article Snippet: TGF-β was neutralized by daily i.p. injection for the indicated time of 150 μg anti–TGF-β Ab (clone 1D11, reactive to mouse TGF-β1/β3; EPIRUS Biopharmaceuticals Netherlands BV).

Techniques: Injection, MANN-WHITNEY

Journal: The Journal of Immunology Author Choice

Article Title: IDO1 and TGF-β Mediate Protective Effects of IFN-α in Antigen-Induced Arthritis

doi: 10.4049/jimmunol.1502125

Figure Lengend Snippet: IFN-α–induced activation of IDO1 in the sensitization phase of AIA and in vitro occurs independently of TGF-β. Female mice were immunized days 1 and 7 with mBSA with or without IFN-α treatment, with or without anti–TGF-β Abs administered i.p. days 1–8 as in Fig. 1 and as described for AIA in Materials and Methods. (A) Sera were collected at days 9 and 28 and analyzed for Trp and Kyn concentration by HPLC. Data are expressed as the ratio of serum levels of Kyn to Trp, n ≥ 7. Comparisons between groups were made by Mann–Whitney U test. (B) Splenocytes isolated day 10 from mBSA-sensitized mice were restimulated ex vivo with 50 μg/ml mBSA with or without 100 U/ml IFN-α, with or without 40 μg/ml anti–TGF-β. Data are expressed as fold change normalized to the reference gene Actb and Ido1 expression in mBSA-stimulated cultured cells from the same mice, n = 5. Paired Student t test was used to evaluate differences between treatments. *p < 0.05.

Article Snippet: TGF-β was neutralized by daily i.p. injection for the indicated time of 150 μg anti–TGF-β Ab (clone 1D11, reactive to mouse TGF-β1/β3; EPIRUS Biopharmaceuticals Netherlands BV).

Techniques: Activation Assay, In Vitro, Concentration Assay, MANN-WHITNEY, Isolation, Ex Vivo, Expressing, Cell Culture

Journal: The Journal of Immunology Author Choice

Article Title: IDO1 and TGF-β Mediate Protective Effects of IFN-α in Antigen-Induced Arthritis

doi: 10.4049/jimmunol.1502125

Figure Lengend Snippet: IFN-α induces IDO1 expression in splenic pDC in vitro and in vivo independently of TGF-β. AIA was induced in female mice with IFN-α treatment, as described in Materials and Methods. At days 4 and 28, mice were sacrificed and pDC were purified from their spleens. (A) Western blot analysis of IDO1 protein expression in pDC. (B) Real-time PCR analysis of Ido1, Tgfb1, Ifna11, and Ifnb1 transcripts in pDC isolated from spleen cells at days 4 and 28 of AIA from mice treated with IFN-α, normalized to the expression of Actb, and presented relative to results of pDC isolated from control mice not treated with IFN-α (dotted line, 1-fold). (C) Splenocytes were isolated at day 10 of AIA, stimulated with 50 μ/ml mBSA plus 250 U/ml IFN-α, with or without anti–TGF-β (40 μg/ml) for 72 h, and analyzed for IDO1-positive pDC by FACS (see Materials and Methods). The bar diagram (left) depicts the percentage of mPDCA+IDO1+ cells among the live lymphocyte population, and the FACS plots (right) show representative dot plots from one of five mice. Data in (A) are the representative of four experiments, and (B) and (C) (mean ± SD, n = 6) were analyzed by Student t test. *p < 0.05, ***p < 0.001.

Article Snippet: TGF-β was neutralized by daily i.p. injection for the indicated time of 150 μg anti–TGF-β Ab (clone 1D11, reactive to mouse TGF-β1/β3; EPIRUS Biopharmaceuticals Netherlands BV).

Techniques: Expressing, In Vitro, In Vivo, Purification, Western Blot, Real-time Polymerase Chain Reaction, Isolation