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mice deficient in cybb, the gene encoding the gp91phox subunit of nox2 (Jackson Laboratory)

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Jackson Laboratory mice deficient in cybb, the gene encoding the gp91phox subunit of nox2

Increased <t>NOX2</t> expression in cisplatin-induced AKI. Three days after cisplatin injection, western blot analysis was used to examine the main NOX family expression in cisplatin-induced AKI. (A) Western blots of NOX1, NOX2, and NOX4. (B–D) Quantitative analysis of NOX2 indicated overexpression compared to WT mice. However, NOX1 and NOX4 decreased after cisplatin injury. (E) Immunofluorescence staining suggests NOX2 expression in the epithelial cells along the renal proximal tubule in cisplatin-induced AKI. NOX2-KO mice did not show NOX2 expression in the normal saline and cisplatin groups. Data represent the mean ± standard error of four mice per group. Scale bar = 50 μM. WT-NS, wild type-normal saline; WT-CDDP, wild type-cisplatin; AQP1: aquaporin 1.

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1) Product Images from "Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation"

Article Title: Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

Journal: Frontiers in Medicine

doi: 10.3389/fmed.2023.1097671

Increased NOX2 expression in cisplatin-induced AKI. Three days after cisplatin injection, western blot analysis was used to examine the main NOX family expression in cisplatin-induced AKI. (A) Western blots of NOX1, NOX2, and NOX4. (B–D) Quantitative analysis of NOX2 indicated overexpression compared to WT mice. However, NOX1 and NOX4 decreased after cisplatin injury. (E) Immunofluorescence staining suggests NOX2 expression in the epithelial cells along the renal proximal tubule in cisplatin-induced AKI. NOX2-KO mice did not show NOX2 expression in the normal saline and cisplatin groups. Data represent the mean ± standard error of four mice per group. Scale bar = 50 μM. WT-NS, wild type-normal saline; WT-CDDP, wild type-cisplatin; AQP1: aquaporin 1.

Figure Legend Snippet: Increased NOX2 expression in cisplatin-induced AKI. Three days after cisplatin injection, western blot analysis was used to examine the main NOX family expression in cisplatin-induced AKI. (A) Western blots of NOX1, NOX2, and NOX4. (B–D) Quantitative analysis of NOX2 indicated overexpression compared to WT mice. However, NOX1 and NOX4 decreased after cisplatin injury. (E) Immunofluorescence staining suggests NOX2 expression in the epithelial cells along the renal proximal tubule in cisplatin-induced AKI. NOX2-KO mice did not show NOX2 expression in the normal saline and cisplatin groups. Data represent the mean ± standard error of four mice per group. Scale bar = 50 μM. WT-NS, wild type-normal saline; WT-CDDP, wild type-cisplatin; AQP1: aquaporin 1.

Techniques Used: Expressing, Injection, Western Blot, Over Expression, Immunofluorescence, Staining, Saline

NOX2-KO mice markedly attenuate the cisplatin-induced ROS increase in WT mice. The glutathione disulfide/glutathione ratio, an indicator of oxidative stress, was increased 3 days after cisplatin injection in the WT group. In contrast, ROS were a significantly blunt in the NOX2-KO CDDP group compared with the WT-CDDP group. Data represent the mean ± standard error of five mice per group. The experiment was repeated twice with similar results.

Figure Legend Snippet: NOX2-KO mice markedly attenuate the cisplatin-induced ROS increase in WT mice. The glutathione disulfide/glutathione ratio, an indicator of oxidative stress, was increased 3 days after cisplatin injection in the WT group. In contrast, ROS were a significantly blunt in the NOX2-KO CDDP group compared with the WT-CDDP group. Data represent the mean ± standard error of five mice per group. The experiment was repeated twice with similar results.

Techniques Used: Injection

Mice with NOX2 deletion had milder cisplatin-induced AKI. (A) Serum creatinine levels indicated that NOX2-KO suppressed the cisplatin-mediated decrease in renal function. (B) BUN levels had a lower trend in NOX2 KO-CDDP mice compared with WT CDDP mice. (C,D) PAS staining of renal tubules revealed cisplatin-induced cast formation, tubular dilatation (black arrow), and tubular epithelial cell injury in WT CDDP mice. Quantitative analysis of PAS staining indicated NOX2 deletion suppressed the tubular injury score 3 days after cisplatin injection. Data represent the mean ± standard error of five mice per group. Scale bar = 100 μM.

Figure Legend Snippet: Mice with NOX2 deletion had milder cisplatin-induced AKI. (A) Serum creatinine levels indicated that NOX2-KO suppressed the cisplatin-mediated decrease in renal function. (B) BUN levels had a lower trend in NOX2 KO-CDDP mice compared with WT CDDP mice. (C,D) PAS staining of renal tubules revealed cisplatin-induced cast formation, tubular dilatation (black arrow), and tubular epithelial cell injury in WT CDDP mice. Quantitative analysis of PAS staining indicated NOX2 deletion suppressed the tubular injury score 3 days after cisplatin injection. Data represent the mean ± standard error of five mice per group. Scale bar = 100 μM.

Techniques Used: Staining, Injection

Mice with NOX2 deletion had decreased Kim-1 levels in cisplatin-induced AKI. (A,B) Kim-1, a biomarker of renal tubular injury, was overexpressed and accumulated in the WT CDDP group’s peritubular area (black arrow). Immunohistochemical analysis indicated that the area of Kim-1 was greater after cisplatin and reduced in the NOX2 KO mice. (C) NOX2 deletion reduced Kim-1 protein levels in cisplatin-induced AKI, as indicated by the Luminex assay. Data represent the mean ± standard error of five mice per group. Scale bar = 100 μM. The experiment was repeated twice with similar results.

Figure Legend Snippet: Mice with NOX2 deletion had decreased Kim-1 levels in cisplatin-induced AKI. (A,B) Kim-1, a biomarker of renal tubular injury, was overexpressed and accumulated in the WT CDDP group’s peritubular area (black arrow). Immunohistochemical analysis indicated that the area of Kim-1 was greater after cisplatin and reduced in the NOX2 KO mice. (C) NOX2 deletion reduced Kim-1 protein levels in cisplatin-induced AKI, as indicated by the Luminex assay. Data represent the mean ± standard error of five mice per group. Scale bar = 100 μM. The experiment was repeated twice with similar results.

Techniques Used: Biomarker Discovery, Immunohistochemical staining, Luminex

Cytokine expression with Luminex assay in cisplatin-induced AKI in the WT and NOX2-KO groups. (A,B) IL-6 and IL-1α proinflammatory factors were significantly reduced in the NOX2 KO-CDDP group compared to the WT-CDDP group. (C–G) MCP-1 and T-helper lymphocyte cytokines such as IFN-γ, IL-4, IL-5, and IL-17A did not show significant changes between the WT-CDDP and NOX2 KO-CDDP groups. (H) IL-10 was significantly reduced in the WT-CDDP group compared with the WT-NS group. IL-10 was mildly recovered in the NOX2 KO-CDDP group compared with the WT-CDDP group. Data represent the mean ± standard error of five mice per group. The experiment was repeated twice with similar results.

Figure Legend Snippet: Cytokine expression with Luminex assay in cisplatin-induced AKI in the WT and NOX2-KO groups. (A,B) IL-6 and IL-1α proinflammatory factors were significantly reduced in the NOX2 KO-CDDP group compared to the WT-CDDP group. (C–G) MCP-1 and T-helper lymphocyte cytokines such as IFN-γ, IL-4, IL-5, and IL-17A did not show significant changes between the WT-CDDP and NOX2 KO-CDDP groups. (H) IL-10 was significantly reduced in the WT-CDDP group compared with the WT-NS group. IL-10 was mildly recovered in the NOX2 KO-CDDP group compared with the WT-CDDP group. Data represent the mean ± standard error of five mice per group. The experiment was repeated twice with similar results.

Techniques Used: Expressing, Luminex

Mice with NOX2 deletion had reduced neutrophil infiltration in cisplatin-induced AKI. (A) Whole kidneys were homogenized into a single-cell suspension for flow cytometric analysis of immune cells. Hierarchical gating was performed to identify Ly6G + , CD11b + neutrophils; F4/80 + , CD11C − macrophages; and F4/80 − , CD11c + dendritic cells. (B,D,E) Neutrophil infiltration was increased on day 3 after cisplatin injection in both WT and NOX2 KO groups. However, the neutrophil percentage of total CD45 + cells was significantly reduced in the NOX2-KO CDDP group on day 3 compared to that of the WT CDDP group. (C,F–I) The percentages of macrophage and dendritic cells among total CD45 + cells were significantly reduced in the WT CDDP group on day 3 compared to the WT on day 0. However, the numbers and percentages of total CD45 + macrophage and dendritic cells were not significantly different between the WT CDDP and NOX2-KO CDDP groups on day 3. Data represent the mean ± standard error of 3–5 mice per group.

Figure Legend Snippet: Mice with NOX2 deletion had reduced neutrophil infiltration in cisplatin-induced AKI. (A) Whole kidneys were homogenized into a single-cell suspension for flow cytometric analysis of immune cells. Hierarchical gating was performed to identify Ly6G + , CD11b + neutrophils; F4/80 + , CD11C − macrophages; and F4/80 − , CD11c + dendritic cells. (B,D,E) Neutrophil infiltration was increased on day 3 after cisplatin injection in both WT and NOX2 KO groups. However, the neutrophil percentage of total CD45 + cells was significantly reduced in the NOX2-KO CDDP group on day 3 compared to that of the WT CDDP group. (C,F–I) The percentages of macrophage and dendritic cells among total CD45 + cells were significantly reduced in the WT CDDP group on day 3 compared to the WT on day 0. However, the numbers and percentages of total CD45 + macrophage and dendritic cells were not significantly different between the WT CDDP and NOX2-KO CDDP groups on day 3. Data represent the mean ± standard error of 3–5 mice per group.

Techniques Used: Suspension, Injection

Cisplatin-induced increase in ICAM-1 and CXCL1 was reduced in NOX2-KO mice. (A,G,H) sICAM expression with Luminex assay was decreased in the NOX2-KO CDDP group compared to the WT CDDP group on day 3, and the area of ICAM-1 labeling (black arrow) through immunohistochemical staining was increased in WT-CDDP but not in NOX2 KO-CDDP mice. (B,C,F) sP-selectin, VEGF, and GM-CSF levels with Luminex assay were not significantly different between the WT CDDP and NOX2-KO CDDP groups on day 3. (D,E) The level of chemokine CXCL1 was significantly lower in the NOX2-KO CDDP group on day 3. However, another chemokine, CXCL2, showed no change between the WT CDDP and NOX2-KO groups. Data represent the mean ± standard error of five mice per group. Scale bar = 100 μM. The experiment was repeated twice with similar results.

Figure Legend Snippet: Cisplatin-induced increase in ICAM-1 and CXCL1 was reduced in NOX2-KO mice. (A,G,H) sICAM expression with Luminex assay was decreased in the NOX2-KO CDDP group compared to the WT CDDP group on day 3, and the area of ICAM-1 labeling (black arrow) through immunohistochemical staining was increased in WT-CDDP but not in NOX2 KO-CDDP mice. (B,C,F) sP-selectin, VEGF, and GM-CSF levels with Luminex assay were not significantly different between the WT CDDP and NOX2-KO CDDP groups on day 3. (D,E) The level of chemokine CXCL1 was significantly lower in the NOX2-KO CDDP group on day 3. However, another chemokine, CXCL2, showed no change between the WT CDDP and NOX2-KO groups. Data represent the mean ± standard error of five mice per group. Scale bar = 100 μM. The experiment was repeated twice with similar results.

Techniques Used: Expressing, Luminex, Labeling, Immunohistochemical staining, Staining

Schematic summarizing the mechanism of NOX2-induced ROS in the renal proximal tubular cells. NOX2 contributes to cisplatin-induced AKI and involves an increase Kim-1 and proinflammatory cytokines, IL6 and IL-1α which also increase neutrophil infiltration with higher endothelial adhesion molecule ICAM-1 and chemokine CXCL1. The box in the figure is NOX2 which has multiple membrane-bound subunits of NADPH oxidase including gp91 phox , p22 phox , p67 phox , p47 phox , and Rac.

Figure Legend Snippet: Schematic summarizing the mechanism of NOX2-induced ROS in the renal proximal tubular cells. NOX2 contributes to cisplatin-induced AKI and involves an increase Kim-1 and proinflammatory cytokines, IL6 and IL-1α which also increase neutrophil infiltration with higher endothelial adhesion molecule ICAM-1 and chemokine CXCL1. The box in the figure is NOX2 which has multiple membrane-bound subunits of NADPH oxidase including gp91 phox , p22 phox , p67 phox , p47 phox , and Rac.

Techniques Used: Membrane

other:

Article Title: Nox2 Regulates Platelet Activation and NET Formation in the Lung
Article Snippet: C57BL/6J (WT) and Nox2-deficient (B6.129S- Cybbtm1Din /J) mice (gp91 phox−/y ) were obtained from Jackson Laboratory (Bar Harbor, ME, USA) and kept in a barrier facility with free access to standard rodent chow and water.

Article Title: Neuroprotective properties of ethanolic extract of Citrus unshiu Markovich peel through NADPH oxidase 2 inhibition in chemotherapy-induced neuropathic pain animal model.
Article Snippet: Funding information Basic Science Research Program, National Research Foundation of Korea (NRF), Korean Government (MSICT), Grant/Award Number: NRF-2019R1F1A1063299 The present study aimed to determine the antioxidant effect of Citrus unshiu Markovich (CUM) extract in neuronal cell lines under oxidative stress and to investigate the effect of chemotherapy-induced peripheral neuropathy (CIPN) on the nociceptive response in a preclinical mice model. We tested the inhibition of H2O2 in Neuro2A cells treated with CUM.. Experimental animals were treated with oxaliplatin to induce CINP, and then administered oral CUM for 4 weeks in order to observe the effect of CUM.. Animals were evaluated weekly for thermal hyperalgesia and digital motor nerve conduction velocity (NCV).

Article Title: Aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in mice.
Article Snippet: NOX2-deficient Cybbtm1din/J mice (Jackson Labs, USA): Slice glucose, NAD(P)H/FAD/pO2 recordings, and lipid peroxidation (MDA) assays.

Article Title: Activation of the MAC1-ERK1/2-NOX2 Pathway Is Required for LPS-Induced Sustaining Reactive Microgliosis, Chronic Neuroinflammation and Neurodegeneration.
Article Snippet: C57BL/6J, B6.129S4-Itgam/J (MAC1 deficient), B6.129P2(SJL)-Myd88/J (MyD88 deficient), and B6.129S-Cybb/J (gp91 deficient) mice were generated by our institute’s animal husbandry staff using breeders obtained from Jackson Laboratories (Bar Harbor, ME, USA).

Article Title: Activation of the MAC1-ERK1/2-NOX2 Pathway Is Required for LPS-Induced Sustaining Reactive Microgliosis, Chronic Neuroinflammation and Neurodegeneration
Article Snippet: C57BL/6J, B6.129S4-Itgam/J (MAC1 deficient), B6.129P2(SJL)-Myd88/J (MyD88 deficient), and B6.129S-Cybb/J (gp91 deficient) mice were generated by our institute’s animal husbandry staff using breeders obtained from Jackson Laboratories (Bar Harbor, ME, USA).

Article Title: Rubicon promotes rather than restricts murine lupus and is not required for LC3-associated phagocytosis
Article Snippet: Cybb-deficient (Catalogue# 002365) mice were purchased from the Jackson Laboratory and backcrossed to the MRL.Faslpr strain for at least 9 generations as previously described (3).

Isolation:

Article Title: Inositol 1,4,5-trisphosphate receptor - reactive oxygen signaling domain regulates excitation-contraction coupling in atrial myocytes.
Article Snippet: .. Atrial myocytes (AMs) were isolated from 3 to 6 month old male WT (C57/BL6) and NOX2 deficient mice (gp91phox deficient: NOX2− /− ; The Jackson Laboratory, Bar Harbor, ME USA [34]). ..

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Journal: Frontiers in Medicine

Article Title: Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

doi: 10.3389/fmed.2023.1097671

Figure Lengend Snippet: Increased NOX2 expression in cisplatin-induced AKI. Three days after cisplatin injection, western blot analysis was used to examine the main NOX family expression in cisplatin-induced AKI. (A) Western blots of NOX1, NOX2, and NOX4. (B–D) Quantitative analysis of NOX2 indicated overexpression compared to WT mice. However, NOX1 and NOX4 decreased after cisplatin injury. (E) Immunofluorescence staining suggests NOX2 expression in the epithelial cells along the renal proximal tubule in cisplatin-induced AKI. NOX2-KO mice did not show NOX2 expression in the normal saline and cisplatin groups. Data represent the mean ± standard error of four mice per group. Scale bar = 50 μM. WT-NS, wild type-normal saline; WT-CDDP, wild type-cisplatin; AQP1: aquaporin 1.

Article Snippet: Mice deficient in Cybb, the gene encoding the gp91phox subunit of NOX2, (B6.129S-Cybbtm1Din/J, No. 002365) were purchased from Jackson Laboratory.

Techniques: Expressing, Injection, Western Blot, Over Expression, Immunofluorescence, Staining, Saline

Journal: Frontiers in Medicine

Article Title: Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

doi: 10.3389/fmed.2023.1097671

Figure Lengend Snippet: NOX2-KO mice markedly attenuate the cisplatin-induced ROS increase in WT mice. The glutathione disulfide/glutathione ratio, an indicator of oxidative stress, was increased 3 days after cisplatin injection in the WT group. In contrast, ROS were a significantly blunt in the NOX2-KO CDDP group compared with the WT-CDDP group. Data represent the mean ± standard error of five mice per group. The experiment was repeated twice with similar results.

Article Snippet: Mice deficient in Cybb, the gene encoding the gp91phox subunit of NOX2, (B6.129S-Cybbtm1Din/J, No. 002365) were purchased from Jackson Laboratory.

Techniques: Injection

Journal: Frontiers in Medicine

Article Title: Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

doi: 10.3389/fmed.2023.1097671

Figure Lengend Snippet: Mice with NOX2 deletion had milder cisplatin-induced AKI. (A) Serum creatinine levels indicated that NOX2-KO suppressed the cisplatin-mediated decrease in renal function. (B) BUN levels had a lower trend in NOX2 KO-CDDP mice compared with WT CDDP mice. (C,D) PAS staining of renal tubules revealed cisplatin-induced cast formation, tubular dilatation (black arrow), and tubular epithelial cell injury in WT CDDP mice. Quantitative analysis of PAS staining indicated NOX2 deletion suppressed the tubular injury score 3 days after cisplatin injection. Data represent the mean ± standard error of five mice per group. Scale bar = 100 μM.

Article Snippet: Mice deficient in Cybb, the gene encoding the gp91phox subunit of NOX2, (B6.129S-Cybbtm1Din/J, No. 002365) were purchased from Jackson Laboratory.

Techniques: Staining, Injection

Journal: Frontiers in Medicine

Article Title: Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

doi: 10.3389/fmed.2023.1097671

Figure Lengend Snippet: Mice with NOX2 deletion had decreased Kim-1 levels in cisplatin-induced AKI. (A,B) Kim-1, a biomarker of renal tubular injury, was overexpressed and accumulated in the WT CDDP group’s peritubular area (black arrow). Immunohistochemical analysis indicated that the area of Kim-1 was greater after cisplatin and reduced in the NOX2 KO mice. (C) NOX2 deletion reduced Kim-1 protein levels in cisplatin-induced AKI, as indicated by the Luminex assay. Data represent the mean ± standard error of five mice per group. Scale bar = 100 μM. The experiment was repeated twice with similar results.

Article Snippet: Mice deficient in Cybb, the gene encoding the gp91phox subunit of NOX2, (B6.129S-Cybbtm1Din/J, No. 002365) were purchased from Jackson Laboratory.

Techniques: Biomarker Discovery, Immunohistochemical staining, Luminex

Journal: Frontiers in Medicine

Article Title: Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

doi: 10.3389/fmed.2023.1097671

Figure Lengend Snippet: Cytokine expression with Luminex assay in cisplatin-induced AKI in the WT and NOX2-KO groups. (A,B) IL-6 and IL-1α proinflammatory factors were significantly reduced in the NOX2 KO-CDDP group compared to the WT-CDDP group. (C–G) MCP-1 and T-helper lymphocyte cytokines such as IFN-γ, IL-4, IL-5, and IL-17A did not show significant changes between the WT-CDDP and NOX2 KO-CDDP groups. (H) IL-10 was significantly reduced in the WT-CDDP group compared with the WT-NS group. IL-10 was mildly recovered in the NOX2 KO-CDDP group compared with the WT-CDDP group. Data represent the mean ± standard error of five mice per group. The experiment was repeated twice with similar results.

Article Snippet: Mice deficient in Cybb, the gene encoding the gp91phox subunit of NOX2, (B6.129S-Cybbtm1Din/J, No. 002365) were purchased from Jackson Laboratory.

Techniques: Expressing, Luminex

Journal: Frontiers in Medicine

Article Title: Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

doi: 10.3389/fmed.2023.1097671

Figure Lengend Snippet: Mice with NOX2 deletion had reduced neutrophil infiltration in cisplatin-induced AKI. (A) Whole kidneys were homogenized into a single-cell suspension for flow cytometric analysis of immune cells. Hierarchical gating was performed to identify Ly6G + , CD11b + neutrophils; F4/80 + , CD11C − macrophages; and F4/80 − , CD11c + dendritic cells. (B,D,E) Neutrophil infiltration was increased on day 3 after cisplatin injection in both WT and NOX2 KO groups. However, the neutrophil percentage of total CD45 + cells was significantly reduced in the NOX2-KO CDDP group on day 3 compared to that of the WT CDDP group. (C,F–I) The percentages of macrophage and dendritic cells among total CD45 + cells were significantly reduced in the WT CDDP group on day 3 compared to the WT on day 0. However, the numbers and percentages of total CD45 + macrophage and dendritic cells were not significantly different between the WT CDDP and NOX2-KO CDDP groups on day 3. Data represent the mean ± standard error of 3–5 mice per group.

Article Snippet: Mice deficient in Cybb, the gene encoding the gp91phox subunit of NOX2, (B6.129S-Cybbtm1Din/J, No. 002365) were purchased from Jackson Laboratory.

Techniques: Suspension, Injection

Journal: Frontiers in Medicine

Article Title: Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

doi: 10.3389/fmed.2023.1097671

Figure Lengend Snippet: Cisplatin-induced increase in ICAM-1 and CXCL1 was reduced in NOX2-KO mice. (A,G,H) sICAM expression with Luminex assay was decreased in the NOX2-KO CDDP group compared to the WT CDDP group on day 3, and the area of ICAM-1 labeling (black arrow) through immunohistochemical staining was increased in WT-CDDP but not in NOX2 KO-CDDP mice. (B,C,F) sP-selectin, VEGF, and GM-CSF levels with Luminex assay were not significantly different between the WT CDDP and NOX2-KO CDDP groups on day 3. (D,E) The level of chemokine CXCL1 was significantly lower in the NOX2-KO CDDP group on day 3. However, another chemokine, CXCL2, showed no change between the WT CDDP and NOX2-KO groups. Data represent the mean ± standard error of five mice per group. Scale bar = 100 μM. The experiment was repeated twice with similar results.

Article Snippet: Mice deficient in Cybb, the gene encoding the gp91phox subunit of NOX2, (B6.129S-Cybbtm1Din/J, No. 002365) were purchased from Jackson Laboratory.

Techniques: Expressing, Luminex, Labeling, Immunohistochemical staining, Staining

Journal: Frontiers in Medicine

Article Title: Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

doi: 10.3389/fmed.2023.1097671

Figure Lengend Snippet: Schematic summarizing the mechanism of NOX2-induced ROS in the renal proximal tubular cells. NOX2 contributes to cisplatin-induced AKI and involves an increase Kim-1 and proinflammatory cytokines, IL6 and IL-1α which also increase neutrophil infiltration with higher endothelial adhesion molecule ICAM-1 and chemokine CXCL1. The box in the figure is NOX2 which has multiple membrane-bound subunits of NADPH oxidase including gp91 phox , p22 phox , p67 phox , p47 phox , and Rac.

Article Snippet: Mice deficient in Cybb, the gene encoding the gp91phox subunit of NOX2, (B6.129S-Cybbtm1Din/J, No. 002365) were purchased from Jackson Laboratory.

Techniques: Membrane

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mice deficient in cybb, the gene encoding the gp91phox subunit of nox2 (Jackson Laboratory)

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