ArticleHypertension (Dallas, Tex. : 1979)2009
Isoforms and functions of NAD(P)H oxidase at the macula densa.
Article in Hypertension (Dallas, Tex. : 1979), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Reactive Oxygen Species (ROS) in Metabolic Disease-Don't Shoot the Metabolic Messenger.International journal of molecular sciences · 2025Review
- Effects of reactive oxygen species on renal tubular transport.American journal of physiology. Renal physiology · 2019Review
- Hydrogen peroxide derived from NADPH oxidase 4- and 2 contributes to the endothelium-dependent vasodilatation of intrarenal arteries.Redox biology · 2018Article
- Role of the Primary Cilia on the Macula Densa and Thick Ascending Limbs in Regulation of Sodium Excretion and Hemodynamics.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Effects of Reactive Oxygen Species on Tubular Transport along the Nephron.Antioxidants (Basel, Switzerland) · 2017Review
- Diabetes and Kidney Disease: Role of Oxidative Stress.Antioxidants & redox signaling · 2016Review
- Macula Densa Nitric Oxide Synthase 1β Protects against Salt-Sensitive Hypertension.Journal of the American Society of Nephrology : JASN · 2016Article
- Inhibition of Nitric Oxide Synthase 1 Induces Salt-Sensitive Hypertension in Nitric Oxide Synthase 1α Knockout and Wild-Type Mice.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Amelioration of nicotinamide adenine dinucleotide phosphate-oxidase mediated stress reduces cell death after blast-induced traumatic brain injury.Translational research : the journal of laboratory and clinical medicine · 2015Article
- Shear stress blunts tubuloglomerular feedback partially mediated by primary cilia and nitric oxide at the macula densa.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- Oxidative status in the macula densa modulates tubuloglomerular feedback responsiveness in angiotensin II-induced hypertension.Acta physiologica (Oxford, England) · 2015Article
- Calcineurin Aβ regulates NADPH oxidase (Nox) expression and activity via nuclear factor of activated T cells (NFAT) in response to high glucose.The Journal of biological chemistry · 2014Article
- Enhanced expression and activity of Nox2 and Nox4 in the macula densa in ANG II-induced hypertensive mice.American journal of physiology. Renal physiology · 2014Article
- NADPH oxidases, reactive oxygen species, and the kidney: friend and foe.Journal of the American Society of Nephrology : JASN · 2013Review
- Mechanism of inhibition of tubuloglomerular feedback by CO and cGMP.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Testosterone enhances tubuloglomerular feedback by increasing superoxide production in the macula densa.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Interaction between nitric oxide and superoxide in the macula densa in aldosterone-induced alterations of tubuloglomerular feedback.American journal of physiology. Renal physiology · 2013Article
- Eplerenone inhibits aldosterone-induced renal expression of cyclooxygenase.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2012Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Macula densa cells produce superoxide (O2-) during tubuloglomerular feedback primarily via NAD(P)H oxidase (NOX). The purpose of the present study was to determine NOXs expressed by the macula densa and the role of each one in NaCl-induced O2- production. To identify which isoforms are expressed, we applied single-cell RT-PCR to macula densa cells isolated by laser capture microdissection and to MMDD1 cells (a macula densa-like cell line). The captured cells expressed neuronal NOS (marker of macula densa), NOX2, and NOX4 but not NOX1. Expression of the NOXs and neuronal NOS was essentially identical in the MMDD1 cells. Thus, we used MMDD1 cells to investigate which isoform is responsible for NaCl-induced O2- production. We used small-interfering RNA to knock down NOX2 or NOX4 in MMDD1 cells and measured O2- exposed to low-salt solution (LS; 70 mmol/L of NaCl) or high-salt solution (HS; 140 mmol/L of NaCl). Exposing control cells (scrambled small-interfering RNA) to HS increased O2- concentrations from 0.75+/-0.28 to 1.48+/-0.46 U/min per 10(5) cells in LS and HS, respectively (P<0.001). Inhibiting NOX2 blocked the HS-induced increase in O2- (0.62+/-0.39 versus 0.76+/-0.31 U/min per 10(5) cells in LS and HS groups, respectively). Blocking NOX4 did not affect HS-induced O2- levels. O2- levels in the control cells during LS and HS were 0.80+/-0.30 and 1.56+/-0.49 U/min per 10(5) cells, respectively (P<0.001); whereas O2- levels in NOX4-small-interfering RNA-treated cells during LS and HS were 0.40+/-0.25 and 1.26+/-0.51 U/min per 10(5) cells, respectively (P<0.001). We conclude that, whereas macula densa cells express the NOX2 and NOX4 isoforms, NOX2 is primarily responsible for NaCl-induced O2- generation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.