anti-p2x1 receptor (extracellular) antibody  (Alomone Labs)

Journal: Cell Biology and Toxicology

Article Title: P2rx1 deficiency alleviates acetaminophen-induced acute liver failure by regulating the STING signaling pathway

doi: 10.1007/s10565-023-09800-1

Figure Lengend Snippet: Knockout of P2rx1 alleviates liver injury in the AILI mouse model. Dynamic hepatic relative P2rx1 mRNA expression and P2RX1 expression in (a) DILI patients and (b) APAP-treated WT mice (n = 4–6 per group); (c) Representative IF staining images of P2RX1 in WT mice with or without AILI (origin magnification × 100, scale bar = 100 μm); (d) Serum ALT and AST levels in WT and P2rx1 −/− mice after a single dose of PBS or APAP (300 mg/kg, n = 4–6 per group); (e) Representative images of H&E staining in liver sections of WT and P2rx1 −/− mice with or without APAP challenge (origin magnification × 100). Quantification of necrotic areas in liver sections by H&E staining (n = 4–6 per group); (f) Survival curve of WT and P2rx1 −/− mice in response to a single lethal dose of APAP (500 mg/kg, n = 12 per group). Data are shown as the means ± SEM, *p < 0.05, **p < 0.01, ***p < 0.001

Article Snippet: As for the materials, incubations were carried out with these primary antibodies specific for P2RX1 (1:200; Alomone), CD11b (1:200; Abcam), MPO (1:300; Abcam), and cleaved-caspase-3 (1:50; Abcam).

Techniques: Knock-Out, Expressing, Staining

Journal: Cell Biology and Toxicology

Article Title: P2rx1 deficiency alleviates acetaminophen-induced acute liver failure by regulating the STING signaling pathway

doi: 10.1007/s10565-023-09800-1

Figure Lengend Snippet: P2rx1 depletion eliminates APAP-induced cell death. (a) Representative images of TUNEL staining (original magnification × 200) and the statistical quantification of TUNEL-positive cells in liver sections of WT and P2rx1 −/− mice with or without APAP treatment (n = 4–6 per group); (b) Western blot and quantification analysis for the expression of hepatic BCL-2 and BCL-XL in WT and P2rx1 −/− mice with or without APAP treatment (n = 3–4); (c) Representative IHC staining (original magnification × 200) and the statistical quantification of hepatic cleaved-caspase-3-positive cells in liver sections of WT and P2rx1 −/− mice with or without APAP treatment (n = 4–6 per group); (d) Caspase-3 activity in the livers with or without APAP treatment (n = 4–6 per group); (e) Representative images of TUNEL staining (original magnification × 200, scale bar = 353 μm) and the quantification of TUNEL-positive primary hepatocytes with or without 5 mM APAP treatment in vitro (n = 3–6 per group). Data are shown as the means ± SEM, *p < 0.05, **p < 0.01, ***p < 0.001

Article Snippet: As for the materials, incubations were carried out with these primary antibodies specific for P2RX1 (1:200; Alomone), CD11b (1:200; Abcam), MPO (1:300; Abcam), and cleaved-caspase-3 (1:50; Abcam).

Techniques: TUNEL Assay, Staining, Western Blot, Expressing, Immunohistochemistry, Activity Assay, In Vitro

Journal: Cell Biology and Toxicology

Article Title: P2rx1 deficiency alleviates acetaminophen-induced acute liver failure by regulating the STING signaling pathway

doi: 10.1007/s10565-023-09800-1

Figure Lengend Snippet: P2rx1 depletion enhances inflammation resolution in response to APAP treatment. (a) Serum TNF-α, IL-6, and MCP-1 levels of both genotypes after PBS or APAP treatment (n = 4–6 per group); (b) Relative hepatic Tnf-α , Il-6 , and Mcp-1 mRNA in both mice after PBS or APAP treatment (n = 4–6 per group); Representative IHC images and the quantification of (c) CD11b-positive cells and (d) MPO-positive cells in liver sections after PBS or APAP treatment (original magnification × 200, n = 4–6 per group). Data are shown as the means ± SEM, *p < 0.05, **p < 0.01

Article Snippet: As for the materials, incubations were carried out with these primary antibodies specific for P2RX1 (1:200; Alomone), CD11b (1:200; Abcam), MPO (1:300; Abcam), and cleaved-caspase-3 (1:50; Abcam).

Techniques:

Journal: Cell Biology and Toxicology

Article Title: P2rx1 deficiency alleviates acetaminophen-induced acute liver failure by regulating the STING signaling pathway

doi: 10.1007/s10565-023-09800-1

Figure Lengend Snippet: P2rx1 depletion improves mitochondria dysfunction and STING signaling-mediated inflammation. (a) RNA-seq analysis of livers from mice 6 h after APAP treatment. Bubble chart showing the top 10 of upregulated and downregulated KEGG enrichment of the significant genes; (b) Enrichment plots from the GSEA analysis; (c) Hepatic MDA and plasma mtDNA levels in both genotypes after PBS or APAP treatment (n = 4–6 per group); (d) JC-1 analysis for mitochondrial membrane potentials in primary hepatocytes after PBS or 5 mM APAP treatment (origin magnification × 100, scale bar = 353 μm); (e) Representative images of MitoSOX Red probe in primary hepatocytes after PBS or 5 mM APAP treatment (origin magnification × 100, scale bar = 353 μm); (f) Western blot analysis for expression of the STING-TBK1-P65 signaling pathway in liver extracts of mice after PBS or APAP treatment. Data are shown as the means ± SEM, *p < 0.05, **p < 0.01

Article Snippet: As for the materials, incubations were carried out with these primary antibodies specific for P2RX1 (1:200; Alomone), CD11b (1:200; Abcam), MPO (1:300; Abcam), and cleaved-caspase-3 (1:50; Abcam).

Techniques: RNA Sequencing Assay, Membrane, Western Blot, Expressing

Journal: Cell Biology and Toxicology

Article Title: P2rx1 deficiency alleviates acetaminophen-induced acute liver failure by regulating the STING signaling pathway

doi: 10.1007/s10565-023-09800-1

Figure Lengend Snippet: STING activator aggravates liver injury of P2rx1 −/− mice after APAP treatment. (a) A schematic of STING activation by DMX (10 mg/kg) in the APAP overdose model. (b) Serum levels of ALT and AST in P2rx1 −/− mice with or without DMX pretreatment (10 mg/kg, n = 4–6 per group); (c) Representative images of H&E staining (original magnification × 100) and quantification of hepatic necrosis area in P2rx1 −/− mice with or without DMX pretreatment (n = 4–6 per group); (d) Representative images and the quantification of TUNEL-positive cells in liver sections of P2rx1 −/− mice with or without DMX pretreatment (original magnification × 200, n = 4–6 per group); (e) Hepatic MDA and (f) plasma mtDNA levels of P2rx1 −/− mice with or without DMX pretreatment; (g) Representative images of MitoSOX Red probe in primary P2rx1 −/− hepatocytes pretreated with DMSO or DMX. Data are shown as the means ± SEM, *p < 0.05, **p < 0.01, ***p < 0.001

Article Snippet: As for the materials, incubations were carried out with these primary antibodies specific for P2RX1 (1:200; Alomone), CD11b (1:200; Abcam), MPO (1:300; Abcam), and cleaved-caspase-3 (1:50; Abcam).

Techniques: Activation Assay, Staining, TUNEL Assay

Journal: Cell Biology and Toxicology

Article Title: P2rx1 deficiency alleviates acetaminophen-induced acute liver failure by regulating the STING signaling pathway

doi: 10.1007/s10565-023-09800-1

Figure Lengend Snippet: STING activator promotes inflammatory response induced by APAP treatment in P2rx1 −/− mice. Representative IHC images and qualification of (a) CD11b-positive cells and (b) MPO-positive cells in the liver tissues of P2rx1 −/− mice with or without DMX pretreatment (origin magnification × 200, n = 4–6 per group); (c) Serum TNF-α, IL-6, and MCP-1 levels of P2rx1 −/− mice with or without DMX pretreatment (n = 4–6 per group); (d) Relative hepatic Tnf-α , Il-6 , and Mcp-1 mRNA levels of P2rx1 −/− mice 6 h with or without DMX pretreatment (n = 4–6 per group); (e) Western blot for the expression of the STING-TBK1-P65 signaling pathway in liver tissues of P2rx1 −/− mice with or without DMX pretreatment. Data are shown as the means ± SEM, **p < 0.01, ***p < 0.001

Article Snippet: As for the materials, incubations were carried out with these primary antibodies specific for P2RX1 (1:200; Alomone), CD11b (1:200; Abcam), MPO (1:300; Abcam), and cleaved-caspase-3 (1:50; Abcam).

Techniques: Western Blot, Expressing