ArticleAmerican journal of physiology. Renal physiology2014
Biomechanical regulation of cyclooxygenase-2 in the renal collecting duct.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Immunolocalization of Sphingolipid Catabolism Enzymes along the Nephron: Novel Early Urinary Biomarkers of Renal Damage.International journal of molecular sciences · 2023Article
- Prostanoid receptors in hyperfiltration-mediated glomerular injury: Novel agonists and antagonists reveal opposing roles for EP2 and EP4 receptors.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Innate Bacteriostatic Mechanisms Defend the Urinary Tract.Annual review of physiology · 2022Review
- Glomerular Biomechanical Stress and Lipid Mediators during Cellular Changes Leading to Chronic Kidney Disease.Biomedicines · 2022Review
- Polymodal roles of TRPC3 channel in the kidney.Channels (Austin, Tex.) · 2020Review
- Prostaglandin E2 stimulates the epithelial sodium channel (ENaC) in cultured mouse cortical collecting duct cells in an autocrine manner.The Journal of general physiology · 2020Article
- TRPC3 determines osmosensitive [Ca2+]i signaling in the collecting duct and contributes to urinary concentration.PloS one · 2019Article
- Mechanotransduction signaling in podocytes from fluid flow shear stress.American journal of physiology. Renal physiology · 2018Article
- Hyperfiltration-associated biomechanical forces in glomerular injury and response: Potential role for eicosanoids.Prostaglandins & other lipid mediators · 2017Review
- Role of biomechanical forces in hyperfiltration-mediated glomerular injury in congenital anomalies of the kidney and urinary tract.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017Review
- Increased urinary prostaglandin E2 metabolite: A potential therapeutic target of Gitelman syndrome.PloS one · 2017Article
- Regulation and function of renal medullary cyclooxygenase-2 during high salt loading.Frontiers in bioscience (Landmark edition) · 2017Review
- Pathophysiology and clinical presentations of salt-losing tubulopathies.Pediatric nephrology (Berlin, Germany) · 2016Review
- Cholesterol affects flow-stimulated cyclooxygenase-2 expression and prostanoid secretion in the cortical collecting duct.American journal of physiology. Renal physiology · 2015Article
- Relative roles of principal and intercalated cells in the regulation of sodium balance and blood pressure.Current hypertension reports · 2015Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
High-dietary sodium (Na), a feature of the Western diet, requires the kidney to excrete ample Na to maintain homeostasis and prevent hypertension. High urinary flow rate, presumably, leads to an increase in fluid shear stress (FSS) and FSS-mediated release of prostaglandin E2 (PGE2) by the cortical collecting duct (CCD) that enhances renal Na excretion. The pathways by which tubular flow biomechanically regulates PGE2 release and cyclooxygenase-2 (COX-2) expression are limited. We hypothesized that FSS, through stimulation of neutral-sphingomyelinase (N-SM) activity, enhances COX-2 expression to boost Na excretion. To test this, inner medullary CD3 cells were exposed to FSS in vitro and mice were injected with isotonic saline in vivo to induce high tubular flow. In vitro, FSS induced N-SM activity and COX-2 protein expression in cells while inhibition of N-SM activity repressed FSS-induced COX-2 protein abundance. Moreover, the murine CCD expresses N-SM protein and, when mice are injected with isotonic saline to induce high tubular flow, renal immunodetectable COX-2 is induced. Urinary PGE2 (445 ± 91 vs. 205 ± 14 pg/ml; P < 0.05) and microdissected CCDs (135.8 ± 21.7 vs. 65.8 ± 11.0 pg·ml(-1)·mm(-1) CCD; P < 0.05) from saline-injected mice generate more PGE2 than sham-injected controls, respectively. Incubation of CCDs with arachidonic acid and subsequent measurement of secreted PGE2 are a reflection of the PGE2 generating potential of the epithelia. CCDs isolated from polyuric mice doubled their PGE2 generating potential and this was due to induction of COX-2 activity/protein. Thus, high tubular flow and FSS induce COX-2 protein/activity to enhance PGE2 release and, presumably, effectuate Na excretion.
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