Journal: JBMR Plus

Article Title: USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy

doi: 10.1093/jbmrpl/ziag004

Figure Lengend Snippet: Deletion of Usp34 accelerates cartilage destruction during TMJ OA. (A) Representative images of Safranin O/Fast Green staining of SHAM and UBR-induced TMJ OA mice. Scale bars: 100 μm for low and 50 μm for high magnification. (B and C) Quantitative analysis regarding cartilage thickness and modified Mankin score according to Safranin O/Fast Green staining. n = 6 per group. (D) Representative micro-CT images reveal the subchondral bone microstructure. Scale bars: 100 μm. (E) Quantitative analysis of subchondral bone parameters. (F and G) Representative images and quantitative analysis of western blot for MMP13, ADAMTS5, α-tubulin in ATDC5 cells transfected with Usp34 siRNA following exposure to IL-1β. (H) Relative mRNA expression of MMP3, MMP13, ADAMTS4, and ADAMTS5 in ATDC5 cells transfected with Usp34 siRNA following exposure to IL-1β.

Article Snippet: To model the inflammatory microenvironment of TMJ OA, ATDC5 cells (1 × 10 5 /well) were cultured in 24-well plates, followed by treatment with 10 ng/mL IL-1β (HY-P7073A; MedChemExpress).

Techniques: Staining, Modification, Micro-CT, Western Blot, Transfection, Expressing

Journal: JBMR Plus

Article Title: USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy

doi: 10.1093/jbmrpl/ziag004

Figure Lengend Snippet: USP34 deubiquitinates and stabilizes ANT1. (A) Volcano plots showing the differentially expressed proteins of USP34-deficient cells from public proteomic dataset in the National Genomics Data Center under accession numbers: OMIX007639. (B) Heatmap showing the differentially expressed protein of USP34-deficient cells from public proteomic dataset (OMIX007639). (C and D) Representative images and quantitative analysis of western blot for ANT1 and α-tubulin in ATDC5 cells transfected with Usp34 siRNA following exposure to IL-1β. (E) Representative images of immunofluorescence staining of ANT1 in the TMJ cartilages of SHAM and UBR-induced TMJ OA mice. Scale bars: 50 μm. (F) Co-immunoprecipitation of USP34 with ectopically expressed ANT1 in HEK293T cells. (G) Immunoblot of ANT1-linked polyubiquitin. HEK293T cells were treated with 10 μM MG132 for 4 h after transfection with the indicated constructs. The cell lysates were subjected to immunoprecipitation with the indicated antibody. (H) Measurement of ANT1 degradation rate. HEK293T cells were transfected with the indicated constructs and treated with 10 mg/mL CHX.

Article Snippet: To model the inflammatory microenvironment of TMJ OA, ATDC5 cells (1 × 10 5 /well) were cultured in 24-well plates, followed by treatment with 10 ng/mL IL-1β (HY-P7073A; MedChemExpress).

Techniques: Western Blot, Transfection, Immunofluorescence, Staining, Immunoprecipitation, Construct

Journal: JBMR Plus

Article Title: USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy

doi: 10.1093/jbmrpl/ziag004

Figure Lengend Snippet: ANT1 overexpression rescues mitochondrial homeostasis in USP34-deficient cells. (A and B) Representative images and quantitative analysis of western blot for LC3, Parkin, PINK1, and α-tubulin in ATDC5 cells transfected with Usp34 siRNA or Lv-ANT1 , following exposure to IL-1β. (C) Representative TEM images of ATDC5 cells transfected with Usp34 siRNA or Lv-ANT1 . Subcellular structures with discernible mitochondria (yellow arrows) and bound by a double limiting membrane are identified as putative mitophagosome structures (red arrows). Scale bars: 200 nm. (D) ATDC5 cells stained with mitotracker and lysotracker after transfection with Usp34 siRNA or Lv-ANT1 . Scale bars: 20 μm. (E) ATDC5 cells stained with Mito-SOX after transfection with Usp34 siRNA or Lv-ANT1 . Scale bars: 20 μm.

Article Snippet: To model the inflammatory microenvironment of TMJ OA, ATDC5 cells (1 × 10 5 /well) were cultured in 24-well plates, followed by treatment with 10 ng/mL IL-1β (HY-P7073A; MedChemExpress).

Techniques: Over Expression, Western Blot, Transfection, Membrane, Staining

Journal: JBMR Plus

Article Title: USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy

doi: 10.1093/jbmrpl/ziag004

Figure Lengend Snippet: USP34 overexpression enhanced chondrocyte viability. (A and B) Representative images and quantitative analysis of western blot for LC3, Parkin, PINK1, and α-tubulin in ATDC5 cells transfected with Usp34 lentiviral activation particles ( Usp34 ac) following exposure to IL-1β. (C and D) Representative images and quantitative analysis of western blot for MMP13, ADAMTS5, and α-tubulin in ATDC5 cells transfected with Usp34 ac following exposure to IL-1β. (E and F) Representative images and quantitative analysis of western blot for MMP13, ADAMTS5, and α-tubulin in ATDC5 cells with the indicated treatment. (G) ATDC5 cells stained with Acan and Col2a1 after transfection with Usp34 ac or Lv-ANT1 . Scale bars: 50 μm. (H and I) Relative mRNA expression of Acan and Col2a1 in ATDC5 cells with the indicated treatments.

Article Snippet: To model the inflammatory microenvironment of TMJ OA, ATDC5 cells (1 × 10 5 /well) were cultured in 24-well plates, followed by treatment with 10 ng/mL IL-1β (HY-P7073A; MedChemExpress).

Techniques: Over Expression, Western Blot, Transfection, Activation Assay, Staining, Expressing

Journal: Cancer Communications

Article Title: The Ly6g high Neutrophil Subset Dictates Breast Cancer Lung Metastasis via CD8 + T Cell Death

doi: 10.34133/cancomm.0003

Figure Lengend Snippet: Il-1β induces Ly6g high neutrophil NETosis in the lung metastatic niche. (A) Heatmap of the scRNA-seq data showing the expression of cytokine genes at different time points during lung metastasis. (B and C) Representative immunofluorescence micrographs (B) showing NET formation by FACS-sorted Ly6g high and Ly6g low neutrophils ( n = 6) after treatment with Il-1β, Cxcl2, and Ccl6 for 6 h in vitro. NETs were stained with antibodies against Mpo (red) and H3cit (green), and nuclei were counterstained with DAPI (blue). The statistical data are presented in (C). (D) Representative immunofluorescence micrographs showing NET formation at the MACRO stages of lung tissue with PBS, rIl-1β, anti-IgG, and anti-Il-1β antibody treatment, respectively [4T1-LM3 (BALB/c) model, n = 5]. NETs were stained with antibodies against Mpo (red) and H3cit (green), and nuclei were counterstained with DAPI (blue). The bar graph on the right quantifies NET formation. (E) Representative bioluminescence imaging and hematoxylin and eosin (H&E) staining images at the MACRO lungs from mice treated with PBS, rIl-1β, IgG, or anti-Il-1β antibody [4T1-LM3 (BALB/c) model, n = 5]. The bar graph on the right shows the quantitative data of lung metastasis burden. (F) Violin plots showing the expression of Il1b in different cell clusters in the lung tissues based on scRNA-seq data from Fig. D. (G) Representative immunofluorescence micrographs demonstrate NET formation in sorted Ly6g high neutrophils ( n = 6). Neutrophils were treated with CM-MΦ or CM-MΦ that had been neutralized with an anti-Il-1β antibody. NETs were stained with antibodies against Mpo (red) and H3cit (green), and nuclei were counterstained with DAPI (blue). (H and I) Mice were treated with anti-IgG control, anti-F4/80 antibody, or anti-F4/80 antibody combined with rIl-1β until the macrometastatic stage [4T1-LM3 (BALB/c) model, n = 6]. (H) Il-1β levels in the lungs were detected by ELISA. (I) Representative immunofluorescence images show NET formation. NETs were stained for Mpo (red) and H3cit (green), and nuclei were counterstained with DAPI (blue). The bar graph on the right quantifies NET formation (I). (J) Macrophages were treated with CM-Neu, NETs (5 μg/ml), NETs (10 μg/ml), or NETs (10 μg/ml) combined with deoxyribonuclease (DNase) I ( n = 3). The expression of Il1b was determined by qPCR. The data with error bars are presented as the mean ± SD; statistical significance was determined by 2-way ANOVA (C) and 1-way ANOVA test (D, E, and G to J). 4T1-LM3, 4T1-lung metastasis 3; ANOVA, analysis of variance; Ccl11 , c-c motif chemokine ligand 11; Ccl12 , c-c motif chemokine ligand 12; Ccl17 , c-c motif chemokine ligand 17; Ccl2 , c-c motif chemokine ligand 2; Ccl22 , c-c motif chemokine ligand 22; Ccl3 , c-c motif chemokine ligand 3; Ccl4 , c-c motif chemokine ligand 4; Ccl5 , c-c motif chemokine ligand 5; Ccl6 , c-c motif chemokine ligand 6; CCL6; c-c motif ligand 6; Ccl9 , c-c motif chemokine ligand 9; CM-MΦ, macrophage-derived conditioned medium; CM-Neu, neutrophil-derived conditioned medium; Cxcl12 , c-x-c motif chemokine ligand 12; Cxcl14 , c-x-c motif chemokine ligand 14; Cxcl16 , c-x-c motif chemokine ligand 16; CXCL2, c-x-c motif chemokine ligand 2; Cxcl2 , c-x-c motif chemokine ligand 2; Cxcl3 , c-x-c motif chemokine ligand 3; Cxcl9 , c-x-c motif chemokine ligand 9; DAPI, 4’,6-diamidino-2-phenylindole; ELISA, enzyme linked immunosorbent assay; FACS, fluorescence-activated cell sorting; H3cit; citrullinated histone H3; Il12a , interleukin 12a; Il13 , interleukin 13; Il18 , interleukin, 18; Il1a , interleukin 1α; Il1b , interleukin 1β; Il-1β, interleukin-1β; Il2 ,interleukin 2; Il33 , interleukin 33; Il4 , interleukin 4; Il6 , interleukin 6; Ly6g, lymphocyte antigen 6 complex locus g; MACRO, macrometastatic lung; MICRO, micrometastatic lung; MPO, myeloperoxidase; NETs, neutrophil extracellular trap; NK, natural killer; NL, normal lung; Ppbp , pro-platelet basic protein; Neu, neutrophil; PRE, premetastatic lung; qRT-PCR, quantitative real-time polymerase chain reaction; rIl-1β, recombinant interleukin-1β; scRNA-seq: single-cell RNA sequencing; SD, standard deviation.

Article Snippet: To induce NET formation, primary tumors were resected on day 21 after the orthotopic injection of 4T1-LM3 cells, followed by daily intraperitoneal injections of recombinant Il-1β (rIl-1β; 8 ng per mouse, HY-P7073, MedChemExpress) until the macrometastatic stage.

Techniques: Expressing, Immunofluorescence, In Vitro, Staining, Imaging, Control, Enzyme-linked Immunosorbent Assay, Derivative Assay, Fluorescence, FACS, Quantitative RT-PCR, Real-time Polymerase Chain Reaction, Recombinant, RNA Sequencing, Standard Deviation

Journal: Cancer Communications

Article Title: The Ly6g high Neutrophil Subset Dictates Breast Cancer Lung Metastasis via CD8 + T Cell Death

doi: 10.34133/cancomm.0003

Figure Lengend Snippet: Prognostic significance of NETs in human BC. (A) Representative FACS plot showing the ratio of human CD84 high and CD84 low neutrophils in healthy individuals ( n = 50) and patients with BC at different stages [stages I/II ( n = 80), stages III/IV ( n = 80)]. To define the CD84 high and CD84 low subsets in humans, we first established the positive gating threshold using FMO controls. Subsequently, the boundary between “high” and “low” subsets was determined based on a clear inflection point observed in the fluorescence intensity histogram. Statistical significance was determined by comparing with the healthy group. The bar graph on the right quantifies the ratio of human CD84 high and CD84 low neutrophils. (B) Representative immunofluorescence micrographs showing NET formation of CD84 high and CD84 low neutrophils, which were sorted by FACS after treatment with PMA for 2 h ( n = 6). NETs were stained with antibodies against MPO (red) and H3cit (green), and nuclei were counterstained with DAPI (blue). The bar graph on the right quantifies the formation of NETs. (C) Plasma NET levels in healthy individuals ( n = 50) and BC patients at different stages [stages I/II ( n = 80), stages III/IV ( n = 80)]. (D) Kaplan–Meier survival curves showing the overall survival (OS) of BC patients with low (NETs < 344.91 pg/ml; n = 83) or high (NETs ≥ 344.91 pg/ml; n = 77) concentrations of plasma NETs. BC patients were stratified into high and low NET groups using the mean plasma NET level of the entire cohort as the cutoff. (E) Receiver operator characteristic (ROC) curve analysis of plasma NET levels for predicting BC patients’ lung metastases ( n = 160). The area under the curve (AUC) value reflects the model’s power to distinguish between BC patients with and without lung metastasis within 6 years after diagnosis. Higher AUC values (approaching 1) denote superior differentiation accuracy at this time point. (F) Correlation between plasma NET levels and CD8 + T cell proportion in healthy individuals and patients with BC ( n = 210). (G) Kaplan–Meier analysis showing the recurrence-free survival of BC patients with high or low levels of LL37 ( n = 4,929). Data were obtained from the Kaplan–Meier plotter database, which does not provide detailed numerical thresholds for LL37 level classification. (H) Mechanism scheme of Ly6g high and Ly6g low neutrophils in promoting pulmonary metastasis of BC. Briefly, Ly6g high neutrophils accumulated in the premetastatic stage and induced CD8 + T cell apoptosis through NETosis. The NET-derived cathelicidin directly bound with Ant1, an mPTP protein in CD8 + T cells, leading to conformational changes in the Ant1 and subsequent Ant1–Vdac1 complex formation, which resulted in mPTP opening, loss of ΔΨm, and uncoupling of mitochondrial electron transport chain in CD8 + T cells. Ly6g low neutrophils bearing MDSC-like transcriptional signatures exhibit a superior capacity to inhibit the proliferation and effector functions of CD8 + T cells. The data with error bars are presented as the mean ± SD; statistical significance was determined by 2-way ANOVA (A), Student’s t test (B), 1-way ANOVA test (C), and 2-sided log-rank test (D and G). 4T1-LM3, 4T1-lung metastasis 3; ANOVA, analysis of variance; APC, allophycocyanin; BC, breast cancer; CD8, cluster of differentiation 8; CD84, cluster of differentiation 84; CI, confidence interval; DAPI, 4',6-diamidino-2-phenylindole; E0771-LM3, E0771-lung metastasis 3; FACS, fluorescence-activated cell sorting; FMO, fluorescence-minus-one; H3cit, citrullinated histone H3; HR, hazard ratio; Interferon-γ, IFN-γ; Il-1β, interleukin-1β; Ly6g, lymphocyte antigen 6 complex locus g; MDSC, myeloid-derived suppressor cell; MPO, myeloperoxidase; mPTP, mitochondrial permeability transition pore; NETs, neutrophil extracellular traps; PADI4, peptidyl arginine deiminase 4; PE, phycoerythrin; PMA, phorbol 12-myristate 13-acetate; RFS, recurrence-free survival; ROS, reactive oxygen species; Vdac1, voltage-dependent anion channel 1; SD, standard deviation; ΔΨm, mitochondrial membrane potential.

Article Snippet: To induce NET formation, primary tumors were resected on day 21 after the orthotopic injection of 4T1-LM3 cells, followed by daily intraperitoneal injections of recombinant Il-1β (rIl-1β; 8 ng per mouse, HY-P7073, MedChemExpress) until the macrometastatic stage.

Techniques: Fluorescence, Immunofluorescence, Staining, Clinical Proteomics, Biomarker Discovery, Derivative Assay, FACS, Permeability, Standard Deviation, Membrane

Journal: Scientific Reports

Article Title: Supramolecular aggregation of aquaporin-4 shapes astrocyte collective migration and mechanics

doi: 10.1038/s41598-026-35900-z

Figure Lengend Snippet: Characterization of the i n vitro model of astrogliosis upon IL-1β/TNF-α exposure. Western Blot ( a ) and densitometric ( b ) analysis of GFAP expression normalized against total protein. Two-way ANOVA with Tukey’s Multiple Comparison test, with n = 10 for each group from N = 5 independent experimental dataset. Refer to Table S1 for details on significant differences between groups and related p -values and Figure S2 for uncropped western blot of GFAP. ( c ) Confocal images of GFAP staining (scale bar: 50 μm). ( d ) Box plot of morphometric analysis based on GFAP positive areas showing an increased area in IL-1β/TNF-α-treated astrocytes compared to controls. Two-way ANOVA with Tukey’s Multiple Comparison test was performed on 10–38 fields, with n ranging from 25 to 41 cells from N = 3 independent experimental dataset. Consult Table S2 for details on significant differences between groups and related p- values.

Article Snippet: Pro-inflammatory cytokines treatment : After 24 h from cell plating, the control medium was replaced with growth medium supplemented with 10 ng/mL TNFα (50,349-MNAE-5) and 10 ng/mL IL-1β (50,101-MNAE-5) (Sino Biological) and replaced every two days for seven days of treatment.

Techniques: Western Blot, Expressing, Comparison, Staining

Journal: Scientific Reports

Article Title: Supramolecular aggregation of aquaporin-4 shapes astrocyte collective migration and mechanics

doi: 10.1038/s41598-026-35900-z

Figure Lengend Snippet: Wound healing assay analysis. ( a ) Representative phase contrast images of cell sheets injured with a wound of ~ 200 µm in length for all conditions at 0 (A-D) and 24 h (E–H) (scale bar: 50 µm). ( b ) Box plots showing wound healing percentages of the scratch wound closure (%). At 6 h, no differences were found between genotypes, but between controls compared to IL-1β/TNF-α-treated astrocytes (**** p < 0.0001). At 12 and 24 h a significant difference was found between WT and OAP-null cells under CTRL conditions (**** p < 0.0001) and between CTRL astrocytes and treated ones (**** p < 0.0001). At each time point (6; 12; 24 h) Two-way ANOVA with Tukey’s Multiple Comparison test was performed on the mean values across the four groups with n ranging from 42 to 51 fields per group and from N = 3 independent experimental datasets.

Article Snippet: Pro-inflammatory cytokines treatment : After 24 h from cell plating, the control medium was replaced with growth medium supplemented with 10 ng/mL TNFα (50,349-MNAE-5) and 10 ng/mL IL-1β (50,101-MNAE-5) (Sino Biological) and replaced every two days for seven days of treatment.

Techniques: Wound Healing Assay, Comparison

Journal: Scientific Reports

Article Title: Supramolecular aggregation of aquaporin-4 shapes astrocyte collective migration and mechanics

doi: 10.1038/s41598-026-35900-z

Figure Lengend Snippet: AQP4 and F-actin staining of injured astrocyte sheets. ( a ) Confocal images (a-o; scale bar: 100 µm) with insets in dashed-lined rectangles (a’-o’; scale bar: 50 µm;) of F-actin (magenta), AQP4 (green) staining, and merged signals of follower cells in migrating astrocytes at 24 h after the scratch (cortical actin: yellow arrow). In IL-1β/TNF-α-treated cells, actomyosin network is profoundly disrupted in randomly dispersed cytoplasmic fibers compared to CTRL astrocytes. ( b ) Proposed model of F-actin rearrangements in leader and follower CTRL cells and unpolarized IL-1β/TNF-α-treated cells (Created in BioRender. Barile, B. (2026) https://BioRender.com/pgn5sgv ).

Article Snippet: Pro-inflammatory cytokines treatment : After 24 h from cell plating, the control medium was replaced with growth medium supplemented with 10 ng/mL TNFα (50,349-MNAE-5) and 10 ng/mL IL-1β (50,101-MNAE-5) (Sino Biological) and replaced every two days for seven days of treatment.

Techniques: Staining

Journal: Scientific Reports

Article Title: Supramolecular aggregation of aquaporin-4 shapes astrocyte collective migration and mechanics

doi: 10.1038/s41598-026-35900-z

Figure Lengend Snippet: AQP4 expression levels and AQP4-mediated water transport kinetics. ( a ) Western Blot analysis of AQP4 expression in CTRL and IL-1β/TNF-α treated WT and OAP-null astrocytes. AQP4 is revealed as two separated bands at ~ 30 kDa (M23-AQP4) and ~ 32 kDa (M1-AQP4) in WT and as one band at ~ 32 kDa (M1-AQP4) in OAP-null astrocyte protein samples. Refer to Figure S3 for uncropped western blots of AQP4. ( b ) Densitometric analysis of the differential expression of M1-AQP4 and M23-AQP4) isoforms normalized against GAPDH for in WT astrocytes and M1-AQP4 isoform expression normalized against total protein in OAP-null astrocytes. Mann–Whitney test, N = 5 independent experimental dataset, n = 10 per each group (* p < 0.05, ** p < 0.001, *** p < 0.001). Both isoforms undergo a statistical significant decrease in IL-1β/TNF-α treated astrocytes compared to CTRL in both genotypes. ( c ) Normalized (F/F0) water transport kinetics of calcein-AM loaded astrocytes upon 60 mOsm/L hypotonic gradient at 20 °C. Curves are representative of N = 3 independent experimental dataset, with n ranging from 28 to 41. ( d ) Box plot showing the fold change of time constants (τ) of cell swelling. Data highlights no significant changes in cell swelling rate upon hypoosmotic challenge in astrocytes exposed to pro-inflammatory stimuli compared to their controls despite a profound change in AQP4 expression. Two-way ANOVA with Tukey’s Multiple Comparison test. Refer to Table S5 for details on significant differences between groups and related p- values. ( e ) Box plot showing the amplitude of cell swelling which is exclusively increased in IL-1β/TNF-α–treated OAP-null cells compared to their controls. Two-way ANOVA with Tukey’s Multiple Comparison test. Refer to Table S6 for details on significant differences between groups and related p- values.

Article Snippet: Pro-inflammatory cytokines treatment : After 24 h from cell plating, the control medium was replaced with growth medium supplemented with 10 ng/mL TNFα (50,349-MNAE-5) and 10 ng/mL IL-1β (50,101-MNAE-5) (Sino Biological) and replaced every two days for seven days of treatment.

Techniques: Expressing, Western Blot, Quantitative Proteomics, MANN-WHITNEY, Comparison

Journal: Scientific Reports

Article Title: Supramolecular aggregation of aquaporin-4 shapes astrocyte collective migration and mechanics

doi: 10.1038/s41598-026-35900-z

Figure Lengend Snippet: Cx43 expression and gap junction-regulated astrocyte connectivity. ( a ) Western Blot of Cx43 expression revealed as two bands at ~ 40 kDa. Refer to Figure S4 for uncropped western blot of Cx43. ( b ) Densitometric analysis of Cx43 normalized against total protein. Data are expressed as mean ± SEM. Two-way ANOVA with Tukey’s Multiple Comparison test, N = 5 independent experimental dataset, n = 10 for each group. Refer to Table S7 for details on significant differences between groups and related p- values. (c) Confocal images of GFAP (magenta) and Cx43 (green) staining (A-D; scale bar: 25 µm). The white boxes indicate the regions imaged by STED microscopy (E–H; scale bar: 5 µm) showing the Cx43-based intercellular junctions. ( d ) Box plot showing Cx43-particle density measured as the number of STED-imaged Cx43-plaques within a 10 µm 2 region. The particle size is significantly decreased in IL-1β/TNF-α-treated astrocytes compared to CTRL cells. Two-way ANOVA with Tukey’s Multiple Comparison test, with n ranging from 14 to 29 fields from N = 3 independent experimental dataset. Refer to Table S8 for details on significant differences between groups and related p- values. ( e ) Box plot showing the size of Cx43-plaques which is greatly reduced in IL-1β/TNF-α-treated astrocytes with respect to controls. Two-way ANOVA with Tukey’s Multiple Comparison test, n ranging from 14 to 29 fields from N = 3 independent experimental dataset. Refer to Table S9 for details on significant differences between groups and related p- values. ( f ) Gap junctional intercellular communication assessed by Lucifer Yellow (LY) scrape loading assay (scale bar = 100 µm). ( g ) Quantification of LY-spreading across the cell sheet expressed as stained area (µm 2 ). Two-way ANOVA with Tukey’s Multiple Comparison test, with n ranging from 40 to 74 fields from N = 2 independent experimental dataset. Refer to Table S10 for details on significant differences between groups and related p- values.

Article Snippet: Pro-inflammatory cytokines treatment : After 24 h from cell plating, the control medium was replaced with growth medium supplemented with 10 ng/mL TNFα (50,349-MNAE-5) and 10 ng/mL IL-1β (50,101-MNAE-5) (Sino Biological) and replaced every two days for seven days of treatment.

Techniques: Expressing, Western Blot, Comparison, Staining, Microscopy