ArticleHypertension (Dallas, Tex. : 1979)2010
Protein kinase C-dependent NAD(P)H oxidase activation induced by type 1 diabetes in renal medullary thick ascending limb.
Article in Hypertension (Dallas, Tex. : 1979), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
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- The AGE-RAGE-oxidative stress axis: A paradigm shift in understanding diabetic retinopathy.Indian journal of ophthalmology · 2026Review
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- miRNA signatures in diabetic retinopathy and nephropathy: delineating underlying mechanisms.Journal of physiology and biochemistry · 2022Review
- Angiotensin II-induced superoxide and decreased glutathione in proximal tubules: effect of dietary fructose.American journal of physiology. Renal physiology · 2020Article
- Quantitative evaluation of skin disorders in type 1 diabetic mice byBiomedical optics express · 2019Article
- Reactive Oxygen Species-Mediated Damage of Retinal Neurons: Drug Development Targets for Therapies of Chronic Neurodegeneration of the Retina.International journal of molecular sciences · 2018Review
- Glycine Protects H9C2 Cardiomyocytes from High Glucose- and Hypoxia/Reoxygenation-Induced Injury via Inhibiting PKCJournal of diabetes research · 2018Article
- Markers and Biomarkers of Endothelium: When Something Is Rotten in the State.Oxidative medicine and cellular longevity · 2017Review
- Free radical scavenging decreases endothelin-1 excretion and glomerular albumin permeability during type 1 diabetes.Physiological reports · 2016Article
- Luminal flow induces NADPH oxidase 4 translocation to the nuclei of thick ascending limbs.Physiological reports · 2016Article
- Receptor for advanced glycation end-products regulates lung fluid balance via protein kinase C-gp91(phox) signaling to epithelial sodium channels.American journal of respiratory cell and molecular biology · 2015Article
- Molecular mechanisms of curcumin on diabetes-induced endothelial dysfunctions: Txnip, ICAM-1, and NOX2 expressions.BioMed research international · 2014Article
- Interaction between NO synthase and NADPH oxidase in control of sodium transport by the renal thick ascending limb during diabetes.Acta physiologica (Oxford, England) · 2013Article
- NADPH oxidase 4 mediates flow-induced superoxide production in thick ascending limbs.American journal of physiology. Renal physiology · 2012Article
- Angiotensin II stimulates superoxide production in the thick ascending limb by activating NOX4.American journal of physiology. Cell physiology · 2012Article
- NADPH oxidase and PKC contribute to increased Na transport by the thick ascending limb during type 1 diabetes.Hypertension (Dallas, Tex. : 1979) · 2012Article
- Article
- Cell signaling through protein kinase C oxidation and activation.International journal of molecular sciences · 2012Review
- Oxidative stress in obstructive nephropathy.International journal of experimental pathology · 2011Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Type 1 diabetes provokes a protein kinase C (PKC)-dependent accumulation of superoxide anion in the renal medullary thick ascending limb (mTAL). We hypothesized that this phenomenon involves PKC-dependent NAD(P)H oxidase activation. The validity of this hypothesis was explored using mTAL suspensions prepared from rats with streptozotocin-induced diabetes and from sham (vehicle-treated) rats. Superoxide production was 5-fold higher in mTAL suspensions from diabetic rats compared with suspensions from sham rats. The NAD(P)H oxidase inhibitor apocynin caused an 80% decrease in superoxide production by mTAL from diabetic rats (P<0.05 vs untreated) without altering superoxide production by sham mTAL. NAD(P)H oxidase activity was >2-fold higher in mTAL from diabetic rats than in sham mTAL (P<0.05). Pretreatment with calphostin C (broad-spectrum PKC inhibitor) or rottlerin (PKCdelta inhibitor) reduced NAD(P)H oxidase activity by approximately 80% in both groups; however, PKCalpha/beta or PKCbeta inhibition did not alter NAD(P)H oxidase activity in either group. Protein levels of Nox2, Nox4, and p47phox were significantly higher in diabetic mTAL than in mTAL from sham rats. In summary, elevated superoxide production by mTAL from diabetic rats was normalized by NAD(P)H oxidase inhibition. PKC-dependent, PKCdelta-dependent, and total NAD(P)H oxidase activity was greater in mTAL from diabetic rats compared with sham. Protein levels of Nox2, Nox4, and p47phox were increased in mTAL from diabetic rats. We conclude that increased superoxide production by the mTAL during diabetes involves a PKCdelta-dependent increase in NAD(P)H oxidase activity in concert with increased protein levels of catalytic and regulatory subunits of the enzyme.
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