ArticleFree radical research2015
Dopamine D1 and D5 receptors differentially regulate oxidative stress through paraoxonase 2 in kidney cells.
Article in Free radical research, 2015. 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, 21 citations in OpenAlex.
- Targeting amino acid metabolic pathways: a novel therapeutic strategy for hyperuricemia-associated complications.Amino acids · 2026Review
- AANAT1 regulates insect midgut detoxification through the ROS/CncC pathway.Communications biology · 2024Article
- Peroxiredoxin-4 and Dopamine D5 Receptor Interact to Reduce Oxidative Stress and Inflammation in the Kidney.Antioxidants & redox signaling · 2023Article
- Examining the role of paraoxonase 2 in the dopaminergic system of the mouse brain.BMC neuroscience · 2022Article
- Inverse Salt Sensitivity of Blood Pressure: Mechanisms and Potential Relevance for Prevention of Cardiovascular Disease.Current hypertension reports · 2022Review
- Dopamine DHypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Renal Dopamine Receptors and Oxidative Stress: Role in Hypertension.Antioxidants & redox signaling · 2021Review
- Dopamine Receptors and the Kidney: An Overview of Health- and Pharmacological-Targeted Implications.Biomolecules · 2021Review
- The Role of the Renal Dopaminergic System and Oxidative Stress in the Pathogenesis of Hypertension.Biomedicines · 2021Review
- Coordinated Contribution of NADPH Oxidase- and Mitochondria-Derived Reactive Oxygen Species in Metabolic Syndrome and Its Implication in Renal Dysfunction.Frontiers in pharmacology · 2021Review
- Lipid rafts are required for effective renal DFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Inactivation of CysBritish journal of pharmacology · 2020Article
- Regulation of monoamine transporters and receptors by lipid microdomains: implications for depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Review
- Developmental expression of paraoxonase 2.Chemico-biological interactions · 2016Article
- Paraoxonase 2 deficiency in mice alters motor behavior and causes region-specific transcript changes in the brain.Neurotoxicology and teratologyArticle
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Authors and funding
9 authors at 4 institutions in 2 countries.
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Abstract
backgroundThe renal dopaminergic system plays an important role in the pathogenesis of hypertension. Dopamine D1-like receptors (D1R and D5R) decrease reactive oxygen species (ROS) production via inhibition of pro-oxidant enzymes such as NADPH oxidase. Paraoxonase 2 (PON2) is also involved in the inhibition of NADPH oxidase activity. Therefore, we tested the hypothesis that D1R and D5R inhibit ROS production by increasing the expression of PON2, including those in membrane microdomains. METHODS AND
resultsPON2 colocalized with D1R and D5R in mouse renal proximal tubules (RPTs), human RPT (hRPT) cells, and HEK293 cells heterologously expressing human D1R (HEK-hD1R) or D5R (HEK-hD5R). Fenoldopam, an agonist for both D1R and D5R, increased PON2 co-immunoprecipitation with D1R and D5R in HEK-hD1R and HEK-hD5R cells, respectively. Silencing PON2 increased ROS production and NADPH oxidase activity, and impaired the inhibitory effect of fenoldopam. Fenoldopam increased PON2 protein in both lipid rafts (LRs) and non-LRs in HEK-hD1R cells, but only in non-LRs in HEK-hD5R and hRPT cells. Long-term (hrs) fenoldopam stimulation increased PON2 protein in a time-dependent manner in HEK-hD5R, but not in HEK-hD1R cells. Because the effects of fenoldopam on non-LR and total PON2 expressions were similar in HEK-hD5R and hRPT cells, additional studies were performed to determine the relationship between D5R and PON2. Renal PON2 protein was decreased in D5(-/-) mice. In hRPT cells, silencing D5R decreased PON2 expression and increased ROS production.
conclusionsWe conclude that D1-like receptors inhibit ROS production by altering PON2 distribution in membrane microdomains in the short-term, and by increasing PON2 expression in the long-term.
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