Journal: The American journal of pathology

Article Title: Macrophages are critical inducers of bleomycin-induced fibrosis in a systemic scleroderma model

doi: 10.1016/j.ajpath.2025.09.009

Figure Lengend Snippet: ( A ) Glycolytic activity was assessed by extracellular acidification rate (ECAR) in BMDM. ( B ) Glycolytic activity was further shown as basal glycolysis (left) and glycolytic capacity (right) by ECAR. ( C ) Oxidative phosphorylation was assessed by oxygen consumption rate (OCR) in BMDM. ( D ) Mitochondrial respiration in BMDM was assessed by OCR, shown as basal respiration (left, OCR pmol/min), maximal respiration (middle, OCR pmol/min), and spare respiratory capacity (right, % OCR). ( E ) Nutrient uptake in BMDM was assessed by flow cytometry, shown as 2NBDG (glucose analog) MFI (left) and BODIPY FL C16 (fatty acid analog) MFI (right). ( F ) Mitochondrial stress in BMDM was assessed by flow cytometry, shown as MTG (mitotracker green, left) and MTO (mitotracker orange, right). ( G ) Reactive oxygen species (ROS) levels in BMDM were measured by flow cytometry and are shown as percentage of ROS + cells (left) and geometric mean fluorescence intensity (MFI, right). ( H ) MerTK mRNA expression was measured by qPCR in BMDM. ( I ) Soluble MER (sMer) in the conditioned medium of BMDM was measured by Western blot. After 72 hours of bleomycin (MacroBLM) or vehicle (MacroCTRL) treatment, cells were washed and incubated for 2 hours in serum-free medium. The conditioned medium was then collected and TCA-precipitated prior to analysis. ( J ) BMDM survival after 72 hours of bleomycin or vehicle treatment was assessed. Cell survival is shown as total cell number (left), Annexin V/7-AAD staining (middle), and calculated viability based on the number of cells plated versus the number of cells remaining after 72 hours (right). ( K ) ADAM17 (sheddase) expression in BMDM was assessed by qPCR (right) and flow cytometry, shown as percentage of ADAM17 + cells (middle) and mean fluorescence intensity (MFI, right). ( L ) Actin cytoskeleton in BMDM was assessed by phalloidin staining and flow cytometry, shown as geometric mean fluorescence intensity (MFI). Panels A–D and I are representative of two independent experiments (n = 4/group for A–D; n = 3–4/group for I; n=4-5/group for L). Panels E, F, G, H, and K are from one experiment (n = 4-5/group). Panel J is from two independent experiments (n = 4–5/group). Data are shown as mean ± SEM. Statistical analysis was performed using Student’s t test (* p < 0.05, ** p < 0.01, *** p < 0.001).

Article Snippet: Primers were obtained from Thermo Fisher: Tgf1 (Mm01227699_m1), MMP2 (Mm00439498_m1), MMP9 (Mm00442991_m1), TIMP1 (Mm01341361_m1), TIMP2 (Mm00441825_m1), Arg1 (Mm00475988_m1), Lyve1 (Mm00475056_m1), Spp1 (Mm00436767_m1), Ctgf (Mm01192933_g1), Vegf (Mm00437306_m1), Egf (Mm00438696_m1), Tnf (Mm00443258_m1), Il1b (Mm00434228_m1), Ccl2 (Mm00441242_m1), Mertk (Mm00434920_m1), Sirpa (Mm00455928_m1), Slc2a1 (Mm00441480_m1), Il6 (Mm00446190_m1), Il10 (Mm01288386_m1), Adam17 (Mm00456428_m1), Lrp1 (Mm00464608_m1), Cd36 (Mm01135198_m1), Axl (Mm00437221_m1), Tyro3 (Mm00444547_m1), Gas6 (Mm00490378_m1), Elmo1 (Mm00519109_m1), Elmo2 (Mm01248046_m1), and Rac1 (Mm01201653_m1).

Techniques: Activity Assay, Phospho-proteomics, Flow Cytometry, Fluorescence, Expressing, Western Blot, Incubation, Staining

Journal: Neural Regeneration Research

Article Title: Fat mass and obesity–mediated N 6 -methyladenosine modification modulates neuroinflammatory responses after traumatic brain injury

doi: 10.4103/NRR.NRR-D-23-01854

Figure Lengend Snippet: ADAM17 is a downstream target of FTO-mediated m6A modification in microglia. (A) The m 6 A-modified genes were significantly different between control and LPS-treated BV2 cells. (B) The overlap between m6A-modified genes and inflammatory response–related genes was analyzed in control and LPS-treated BV2 cells using Venn diagrams. (C) Volcano plot of the gene enrichment pathway in control and LPS-treated BV2 cells. Compared with the control group, LPS-treated BV2 cells induced an up-regulation of the downstream effector molecules of the ADAM17/TNF-α/NF-κB pathway, including ADAM17, RELA and TNF-α. (D) m6A RNA-sequencing profile of the control and LPS-treated BV2 cells. By comparing m 6 A-sequencing with control BV2 cells, ADAM17, TNF-α and RELA mRNA in LPS-treated BV2 cells mainly concentrated in the coding sequences and 3′-UTR regions. (E, F) Compared with siFTO, siFTO + LPS BV2 cells, the levels of ADAM17, TNF-α, and RELA mRNA in oeFTO, oeFTO + LPS BV2 cells decreased (E) and protein levels also decreased (F). Values are expressed as mean ± SD from at least three independent experiments and the dots represent the value of each experiment. ** P < 0.01, *** P < 0.001 (one-way analysis of variance followed by Student–Newman–Keuls tests). ADAM17: A disintegrin and metalloproteases 17; FTO: the fat mass and obesity-related protein; LPS: lipopolysaccharides; mRNA: messenger ribonucleic acid; m 6 A: N 6 -methyladenosine; N.S.: not significant; NF-κB: nuclear factor kappa B; RELA: v-rel avian reticuloendotheliosis viral oncogene homolog A; TNF-α: tumor necrosis factor-α; UTR: untranslated region.

Article Snippet: In some experiments, transfected BV2 cells were treated with the ADAM17 inhibitor TAPI-1 (1 μM; MedChemExpress, Monmouth Junction, NJ, USA) for another 48 hours at 37°C.

Techniques: Modification, Control, RNA Sequencing, Sequencing

Journal: Neural Regeneration Research

Article Title: Fat mass and obesity–mediated N 6 -methyladenosine modification modulates neuroinflammatory responses after traumatic brain injury

doi: 10.4103/NRR.NRR-D-23-01854

Figure Lengend Snippet: The epigenetic regulation of ADAM17 in an FTO-m 6 A-dependent mechanism. (A) Detection of ADAM17 precursor (pre-ADAM17) and mature transcripts (mat-ADAM17) by quantitative real-time polymerase chain reaction. The mat-ADAM17 mRNA was significantly enhanced in siFTO BV2 cells compared with oeFTO BV2 cells. (B) Detection of the half-life of ADAM17 in oeFTO and siFTO BV2 cells pretreated with actinomycin D and analyzed at 0, 2, 4, 6 and 8 hours. (C) The oeFTO and siFTO BV2 cells were pretreated with cycloheximide for 90 minutes; western blot analysis showed that ADAM17 protein had a longer half-life in the siFTO BV2 cells. (D) Schematic representation of positions of the m 6 A motifs within ADAM17 mRNA. (E) Schematic representation of the mutated (GGAC to GGTC) 3′-UTR pmirGLO vectors. (F) BV2 cells were transfected with pmirGLO-3′-UTR (wildtype, WT) or pmirGLO-3′-UTR-Mut1/2/3 (mutant, MUT1/2/3) reporter plasmids. The MUT3 construct had markedly decreased luciferase activity compared with WT BV2 cells. Values are expressed as mean ± SD from at least three independent experiments and the dots represent the value of each experiment. ** P < 0.01, *** P < 0.001 (one-way analysis of variance followed by Student–Newman–Keuls tests). ADAM17: A disintegrin and metalloproteases 17; FTO: the fat mass and obesity-related protein; mRNA: messenger ribonucleic acid; N.S.: not significant; m6A: N6-methyladenosine; UTR: untranslated region.

Article Snippet: In some experiments, transfected BV2 cells were treated with the ADAM17 inhibitor TAPI-1 (1 μM; MedChemExpress, Monmouth Junction, NJ, USA) for another 48 hours at 37°C.

Techniques: Real-time Polymerase Chain Reaction, Western Blot, Transfection, Mutagenesis, Construct, Luciferase, Activity Assay

Journal: Neural Regeneration Research

Article Title: Fat mass and obesity–mediated N 6 -methyladenosine modification modulates neuroinflammatory responses after traumatic brain injury

doi: 10.4103/NRR.NRR-D-23-01854

Figure Lengend Snippet: Inhibition of ADAM17 in vitro blocks microglial activation after FTO-m6A modification. (A, B) In situ hybridization results indicated that ADAM17 co-localized with FTO in oeFTO and siFTO BV2 cells treated with or without LPS. (A) Double staining of FISH and IF demonstrated that FTO overexpression combined with LPS stimulus increased the co-localization of FTO protein and ADAM17 mRNA. Scale bars: 20 µm. (B) Line profile of colocalization. (C, D) M1-like (CD86 + /Iba-1 + ) microglia in the siFTO + TAPI group decreased compared with the siFTO group (C). Scale bars: 50 µm. The protein levels of CD86, ADAM17, and iNOS were down-regulated, while the expression of CD206 and Arg-1 increased in the siFTO + TAPI group (D). (E) ELISA results showed that the siFTO + TAPI group had significantly reduced expression of IL-1β, TNF-α, and IL-6 and increased expression of TGF-β1 compared with the siFTO group. Values are expressed as mean ± SD from at least three independent experiments and the dots represent the value of each experiment. * P < 0.05, ** P < 0.01, *** P < 0.001 (one-way analysis of variance followed by Student–Newman–Keuls tests). ADAM17: A disintegrin and metalloproteases 17; CD: cluster of differentiation; ELISA: enzyme-linked immunosorbent assay; FISH: fluorescence in situ hybridization; FTO: the fat mass and obesity-related protein; Iba-1: ionized calcium-binding adapter molecule 1; IF: immunofluorescence; iNOS: inducible nitric oxide synthase; IL-1β: interleukin-1β; LPS: lipopolysaccharides; N.S.: not significant; TGF-β1: transforming growth factor-β1; TNF-α: tumor necrosis factor-α.

Article Snippet: In some experiments, transfected BV2 cells were treated with the ADAM17 inhibitor TAPI-1 (1 μM; MedChemExpress, Monmouth Junction, NJ, USA) for another 48 hours at 37°C.

Techniques: Inhibition, In Vitro, Activation Assay, Modification, In Situ Hybridization, Double Staining, Over Expression, Expressing, Enzyme-linked Immunosorbent Assay, Fluorescence, Binding Assay, Immunofluorescence

Journal: Neural Regeneration Research

Article Title: Fat mass and obesity–mediated N 6 -methyladenosine modification modulates neuroinflammatory responses after traumatic brain injury

doi: 10.4103/NRR.NRR-D-23-01854

Figure Lengend Snippet: Enhancement of FTO reduces neuronal apoptosis and inhibits neuroinflammation after TBI in vivo. (A, B) The percentage of apoptotic cells determined by Nissl staining was higher in the TBI group than in the sham group. The neuronal apoptosis rate in the TBI + NADP group was significantly lower on day 3 after TBI compared with the TBI group. The arrows indicate apoptotic neurons. Scale bars: 50 µm. (C) Western blot analysis revealed the upregulation of apoptotic factors (caspase-3 and Bax) in the injured cortex on day 3 after TBI. The levels of cleaved caspase-3 and Bax in the TBI + NADP group were decreased compared with the TBI group, and the anti-apoptotic factor Bcl-2 was increased. (D) The M1-like microglial polarization was inhibited in the TBI + NADP group. Representative photomicrographs of M1-like (CD86 + , red, Alexa FluorTM 647/Iba-1 + , green, Alexa FluorTM 488) microglia are shown. Scale bars: 50 µm. (E) The TBI + NADP group showed significantly reduced expression of ADAM17, CD86, and iNOS and increased the expression of CD206 and Arg-1 compared with the TBI group. (F) ELISA results showed that the TBI + NADP group showed significantly reduced expression of TNF-α, IL-1β, IL-6 and IFN-γ compared with the TBI group. Values are expressed as mean ± SD from at least three independent experiments and the dots represent the value of each experiment. * P < 0.05, ** P < 0.01, *** P < 0.001 (one-way analysis of variance followed by Student–Newman–Keuls tests). ADAM17: A disintegrin and metalloproteases 17; Arg-1: arginase-1; Bcl-2: B-cell lymphoma-2; Bax: BCL2-Associated X; CD: cluster of differentiation; ELISA: enzyme-linked immunosorbent assay; FTO: the fat mass and obesity-related protein; Iba-1: ionized calcium-binding adapter molecule 1; IFN-γ: interferon-γ; IL-1β: interleukin-1β; iNOS: inducible nitric oxide synthase; N.S.: not significant; NADP: nicotinamide adenine dinucleotide phosphate; TBI: traumatic brain injury.

Article Snippet: In some experiments, transfected BV2 cells were treated with the ADAM17 inhibitor TAPI-1 (1 μM; MedChemExpress, Monmouth Junction, NJ, USA) for another 48 hours at 37°C.

Techniques: In Vivo, Staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Binding Assay

Journal: Neural Regeneration Research

Article Title: Fat mass and obesity–mediated N 6 -methyladenosine modification modulates neuroinflammatory responses after traumatic brain injury

doi: 10.4103/NRR.NRR-D-23-01854

Figure Lengend Snippet: FTO regulates neuroinflammation in vivo by targeting ADAM17 in microglia after TBI. (A) Western blotting demonstrated that NADP intervention inhibited ADAM17, TNF-α, and NF-κB p65. (B) Schematic illustration of the isolation of exosomes in the supernatant of NC and oeADAM17 BV2 cells; exosomes were isolated and characterized through TEM, NTA, and exosomal biomarkers assay. Scale bars: 200 nm. (C) Compared with the TBI + NADP group, the TBI + NADP + exo-oeADAM17 group showed significantly increased expression of ADAM17, CD86, and iNOS and decreased the expression of CD206 and Arg-1. (D) ELISA results showed that the TBI + NADP + exo-oeADAM17 group showed significantly increased expression of TNF-α, IL-1β, IL-6 and IFN-γ. (E) The apoptosis rate of neurons in the TBI + NADP + exo-oeADAM17 group was significantly higher than that in the TBI + NADP group on day 3 after TBI. Representative photomicrographs of the Nissl-stained neurons are shown. The arrows indicate apoptotic neurons. Scale bar: 50 µm. (F) Representative photos of Evans blue dye extravasation. Values are expressed as mean ± SD from at least three independent experiments and the dots represent the value of each experiment. ** P < 0.01, *** P < 0.001 (one-way analysis of variance followed by Student Newman–Keuls tests). ADAM17: A disintegrin and metalloproteases 17; Arg-1: arginase-1; Bcl-2: B-cell lymphoma-2; Bax: BCL2-Associated X; CD: cluster of differentiation; ELISA: enzyme-linked immunosorbent assay; FTO: the fat mass and obesity-related protein; Iba-1: ionized calcium-binding adapter molecule 1; IFN-γ: interferon-γ; IL-1β: interleukin-1β; iNOS: inducible nitric oxide synthase; NADP: nicotinamide adenine dinucleotide phosphate; NC: negative control; NF-κB: nuclear factor kappa-B; NTA: nanoparticle tracking analysis; N.S.: not significant; TEM: transmission electron microscope; TBI: traumatic brain injury; TNF-α: tumor necrosis factor-α.

Article Snippet: In some experiments, transfected BV2 cells were treated with the ADAM17 inhibitor TAPI-1 (1 μM; MedChemExpress, Monmouth Junction, NJ, USA) for another 48 hours at 37°C.

Techniques: In Vivo, Western Blot, Isolation, Expressing, Enzyme-linked Immunosorbent Assay, Staining, Binding Assay, Negative Control, Transmission Assay, Microscopy

Journal: bioRxiv

Article Title: Endothelial ADAM17 Promotes Neutrophil Migration and Pulmonary Microvascular Permeability in ARDS

doi: 10.64898/2026.01.21.700786

Figure Lengend Snippet: (A) Gene expression of ADAM17 in lung tissue three hours after LPS inhalation, measured by RT-qPCR (n = 4/4/14/8 mice per group). Expression data were normalized to the ADAM17 fl/fl Tie2-Cre − LPS control group, whose mean value was set to 1. (B) Quantification of ADAM17 mean fluorescence intensity (MFI) in lung tissue using LasX software (n = 4 mice per group; 10 measurements per image). (C) Representative z-stack immunofluorescence images showing ADAM17 expression in lung tissue under the indicated conditions (original magnification ×63). Data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with appropriate post hoc testing; *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: Sections were then incubated with primary antibodies targeting ADAM17 (rabbit anti-ADAM17, polyclonal, Bioss, USA), Ly6G/C (rat anti-Ly6G/C, clone RB6-8C5, Abcam, UK), VE-Cadherin (goat anti-VE-Cadherin, polyclonal, R&D Systems, USA), TNFR1 (mouse anti-TNFR1, clone H-5, Santa Cruz, USA), IL-6Rα (mouse anti-IL-6Rα, clone H-7, Santa Cruz, USA), and vWF (sheep anti-vWF, polyclonal, Abcam, UK) followed by incubation with the corresponding fluorescently labelled secondary antibodies including Alexa Fluor 488 goat anti-rabbit, Alexa Fluor 647 goat anti-rat, Alexa Fluor 488 donkey anti-goat, Alexa Fluor 594 goat anti-mouse, Alexa Fluor 488 donkey anti-mouse and Alexa Fluor 647 donkey anti-sheep.

Techniques: Gene Expression, Quantitative RT-PCR, Expressing, Control, Fluorescence, Software, Immunofluorescence

Journal: bioRxiv

Article Title: Endothelial ADAM17 Promotes Neutrophil Migration and Pulmonary Microvascular Permeability in ARDS

doi: 10.64898/2026.01.21.700786

Figure Lengend Snippet: Endothelial ADAM17 enhances neutrophil migration into the inflamed lung. (A–D) Representative immunohistochemical images showing polymorphonuclear neutrophil (PMN) distribution in lung tissue under the indicated conditions. PMNs were stained using an anti-Ly6G+C antibody (brown) with hematoxylin counterstain. Red arrows indicate PMNs (n = 4 mice per group; original magnification ×20). (E) Quantification of PMNs per high-power field (HPF; n = 4 mice per group, 10 images per group). (F–I) Flow cytometric quantification of PMNs in blood (F), adherent to the pulmonary endothelium (G), within the interstitium (H), and in BAL fluid (I) 24 hours after LPS inhalation (n = 4/4/12–14/8). (J–L) Quantification of CD162 (PSGL-1) MFI and (M–O) CD49d MFI on PMNs isolated from blood, lung, and BAL Data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA.

Article Snippet: Sections were then incubated with primary antibodies targeting ADAM17 (rabbit anti-ADAM17, polyclonal, Bioss, USA), Ly6G/C (rat anti-Ly6G/C, clone RB6-8C5, Abcam, UK), VE-Cadherin (goat anti-VE-Cadherin, polyclonal, R&D Systems, USA), TNFR1 (mouse anti-TNFR1, clone H-5, Santa Cruz, USA), IL-6Rα (mouse anti-IL-6Rα, clone H-7, Santa Cruz, USA), and vWF (sheep anti-vWF, polyclonal, Abcam, UK) followed by incubation with the corresponding fluorescently labelled secondary antibodies including Alexa Fluor 488 goat anti-rabbit, Alexa Fluor 647 goat anti-rat, Alexa Fluor 488 donkey anti-goat, Alexa Fluor 594 goat anti-mouse, Alexa Fluor 488 donkey anti-mouse and Alexa Fluor 647 donkey anti-sheep.

Techniques: Migration, Immunohistochemical staining, Staining, Isolation

Journal: bioRxiv

Article Title: Endothelial ADAM17 Promotes Neutrophil Migration and Pulmonary Microvascular Permeability in ARDS

doi: 10.64898/2026.01.21.700786

Figure Lengend Snippet: (A) Schematic overview of ADAM17 maturation and intracellular transport. (B–D) Schematic representations of TNFR1/2 (B) , IL-6R (C) , and TLR4 (D) signaling pathways. (E) RT-qPCR-based gene expression analysis of inflammatory signaling components in murine lung tissue three hours after LPS inhalation (n = 4/4/10–14/6–8). (F–G) Quantification of TNFR1 (F) and IL-6Rα (G) MFI in lung tissue using LasX (n = 4 mice per group; 10 measurements per image). Data are presented as mean ± SD; Statistical analysis: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, using one-way ANOVA.

Article Snippet: Sections were then incubated with primary antibodies targeting ADAM17 (rabbit anti-ADAM17, polyclonal, Bioss, USA), Ly6G/C (rat anti-Ly6G/C, clone RB6-8C5, Abcam, UK), VE-Cadherin (goat anti-VE-Cadherin, polyclonal, R&D Systems, USA), TNFR1 (mouse anti-TNFR1, clone H-5, Santa Cruz, USA), IL-6Rα (mouse anti-IL-6Rα, clone H-7, Santa Cruz, USA), and vWF (sheep anti-vWF, polyclonal, Abcam, UK) followed by incubation with the corresponding fluorescently labelled secondary antibodies including Alexa Fluor 488 goat anti-rabbit, Alexa Fluor 647 goat anti-rat, Alexa Fluor 488 donkey anti-goat, Alexa Fluor 594 goat anti-mouse, Alexa Fluor 488 donkey anti-mouse and Alexa Fluor 647 donkey anti-sheep.

Techniques: Protein-Protein interactions, Quantitative RT-PCR, Gene Expression

Journal: bioRxiv

Article Title: Endothelial ADAM17 Promotes Neutrophil Migration and Pulmonary Microvascular Permeability in ARDS

doi: 10.64898/2026.01.21.700786

Figure Lengend Snippet: Flow cytometric analysis of PMN distribution across lung compartments—blood (A) , endothelial-adherent (B) , interstitial (C) , and BAL (D) -24 hours after LPS inhalation with or without systemic ADAM17 inhibition (n = 4/13–14/7/7). (E) Quantification of CXCL2/3 in BAL fluid three hours after LPS inhalation by ELISA (n = 4/12/7/7). (F) Quantification of JAM-A MFI on pulmonary endothelial cells 24 hours after LPS inhalation (n = 4/14/7/7). (G) Quantification of VE-cadherin MFI in lung tissue using LasX (n = 4 mice per group; 10 measurements per image). (H–I) Photometric quantification of Evans blue in plasma (H) and lung tissue (I) six hours after LPS inhalation (n = 4/11/7/6–7). The data shown for ADAM17 fl/fl Tie2-Cre - controls were previously presented in the following panels: in , in , in , and in (to minimize animal numbers in accordance with the 3R principle). Data are presented as mean ± SD; Statistical analysis: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, using one-way ANOVA.

Article Snippet: Sections were then incubated with primary antibodies targeting ADAM17 (rabbit anti-ADAM17, polyclonal, Bioss, USA), Ly6G/C (rat anti-Ly6G/C, clone RB6-8C5, Abcam, UK), VE-Cadherin (goat anti-VE-Cadherin, polyclonal, R&D Systems, USA), TNFR1 (mouse anti-TNFR1, clone H-5, Santa Cruz, USA), IL-6Rα (mouse anti-IL-6Rα, clone H-7, Santa Cruz, USA), and vWF (sheep anti-vWF, polyclonal, Abcam, UK) followed by incubation with the corresponding fluorescently labelled secondary antibodies including Alexa Fluor 488 goat anti-rabbit, Alexa Fluor 647 goat anti-rat, Alexa Fluor 488 donkey anti-goat, Alexa Fluor 594 goat anti-mouse, Alexa Fluor 488 donkey anti-mouse and Alexa Fluor 647 donkey anti-sheep.

Techniques: Inhibition, Enzyme-linked Immunosorbent Assay, Clinical Proteomics

Journal: Canadian Respiratory Journal

Article Title: TAPI‐1 Combined With Silicone Stents Alleviated Severe Traumatic Tracheal Stenosis via the ADAM17/TGF‐β1 Pathway

doi: 10.1155/carj/9485331

Figure Lengend Snippet: The proliferation of tracheal epithelial cells induced by GM‐CSF was inhibited by lentivirus‐mediated ADAM17 RNAi.

Article Snippet: After blocking with 5% skim milk at room temperature for 1 h, the membranes were incubated with the following primary antibodies at 4°C for 12 h: ADAM17 (29948‐1‐AP; Proteintech, USA), TGF‐β1 (21898‐1‐AP; Proteintech, USA), fibronectin (15613‐1‐AP; Proteintech, USA), and β‐actin antibody (D110001‐0100; Sangon, Shanghai, China), all at a dilution of 1:1000.

Techniques: