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PMID |
Sentence |
1 |
15993337
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Eight weeks after streptozotocin treatment, we found a doubling in nox1 protein expression, while the expression of nox4 remained unchanged.
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2 |
15998257
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Overexpression of Nox4 also significantly reversed the inhibition of insulin-stimulated receptor tyrosine phosphorylation by PTP1B, a widely expressed PTPase implicated in the negative regulation of insulin signaling, by inhibiting its catalytic activity.
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3 |
17462535
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AGE differentially regulated VSMC NADPH oxidase catalytic subunits, stimulating the transcription of Nox1 (201+/-12.7%, p<0.0001), while having no effect on Nox4.
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4 |
20651026
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Moreover, ezetimibe also reduced vascular superoxide levels in db/db mice, accompanied by the attenuation of NADPH oxidase subunit gp91(phox) and Nox4 and the prevention of down-regulation of Cu/Zn-superoxide dismutase (SOD) and extracellular SOD.
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5 |
20828387
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In their heart PPAR gamma, tissue inhibitor of metalloproteinase-4 (TIMP-4) and anti-oxidant thioredoxin were attenuated whereas matrix metalloproteinase (MMP)-9, TIMP-3 and NADPH oxidase 4 (NOX4) were induced.
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6 |
20861022
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Here, we show that HG inactivates AMP-activated protein kinase (AMPK), up-regulates Nox4, enhances NADPH oxidase activity, and induces podocyte apoptosis.
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7 |
20861022
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Activation of AMPK blocked HG-induced expression of Nox4, NADPH oxidase activity, and apoptosis.
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8 |
20861022
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Inactivation of AMPK by HG up-regulated the expression and phosphorylation of p53, and p53 acted downstream of Nox4.
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9 |
20861022
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Glomeruli isolated from these mice showed decreased phosphorylation of AMPK and enhanced expression of Nox4 and p53.
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10 |
20861022
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Our results uncover a novel function of AMPK that integrates metabolic input to Nox4 and provide new insight for activation of p53 to induce podocyte apoptosis.
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11 |
20630933
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Expression (gene and protein) of Nox4, p22(phox), and p47(phox), but not Nox1 or Nox2, was increased in kidney cortex, but not medulla, from db/db vs. control mice (db/m) (P < 0.05).
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12 |
21071935
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Therefore, the present study was to test whether miRNAs importantly contribute to the regulation of NOX4 expression, a major catalytic subunit of NADPH oxidase under hyperglycemia. diabetic rats were induced by streptozotocin. miRNA microarray, Western blot, real-time RT-PCR and luciferase reporter assays were employed in this study. among 5 miRNAs, which are predicted to have a binding capacity to rat NOX4, the miRNA-25 level was significantly reduced both in the kidney from diabetic rats and in high glucose-treated mesangial cells, accompanied by the increases in NOX4 expression levels.
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13 |
21071935
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We then showed that miR-25 negatively regulated NOX4 expression by directly targeting the 3'-UTR by luciferase reporter assays.
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14 |
21071935
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It was found that transfection of miR-25 precursor significantly decreased the luciferase activity of NOX4 3'-UTR by 39.5%, whereas the mutant sequence restored levels to 79.4%.
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15 |
21239445
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Nox4 knockdown, which is reportedly to produce ROS in insulin signaling, attenuated IGF-I-induced IGF-IR phosphorylation, indicating that Nox4 is involved in the regulation of IGF-I signaling.
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16 |
20489161
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SM-caPTH1R downregulated aortic Col1A1, Runx2, and Nox1 expression without altering TNF, Msx2, Wnt7a/b, or Nox4.
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17 |
19019916
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Exposure of MCs to AOPPs, through membrane-associated phosphorylation of PKCalpha, induced rapid phosphorylation of cytosolic p47(phox) and its membrane translocation, enhanced interaction of p47(phox) with the membrane components p22(phox) and Nox4, and increased expression of these key regulatory subunits of NADPH oxidase.
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18 |
21503956
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We found long-term (3 and 5 days) exposure of mouse podocytes to high glucose concentrations caused oxidative stress, as evidenced by increased expression of Nox4 and activities of NAD(P)H oxidase (? 182%) and SOD (? 39%) and decreased activities of GPx (? -40%) and CAT (? -35%).
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19 |
20332345
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Overexpression of Nox4 increased basal level of ROS generation, HIF-1alpha, and VEGF expression in RCECs.
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20 |
20332345
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Moreover, inhibition of Nox4 attenuated hypoxia-induced upregulation of HIF-1alpha and high-glucose-elicited phosphorylation of STAT3.
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21 |
20332345
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Finally, depletion of Nox4 by adenovirus-delivered Nox4 small interfering RNA significantly decreased retinal NADPH oxidase activity and VEGF expression and reduced retinal vascular premeability in db/db mice.
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22 |
20332345
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Activation of Nox4 plays an important role in high-glucose- and hypoxia-mediated VEGF expression and diabetes-induced BRB breakdown.
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23 |
21729693
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Results showed that in HEC incubated with AGE-LDL, Am led to: (i) decrease of the oxidative stress: by reducing p22(phox), NOX4, iNOS expression, NADPH oxidase activity, 4-HNE and 3-nitrotyrosine levels; (ii) decrease of the inflammatory stress: by the reduction of MCP-1 and VCAM-1 expression, as well as of the number of monocytes adhered to HEC; (iii) inhibition of ROS-sensitive signalling pathways: by decreasing phosphorylation of p38 MAPK and p65 NF-?B subunits.
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