ArticleTransplantation2015
Stimulation of Dopamine D3 Receptor Attenuates Renal Ischemia-Reperfusion Injury via Increased Linkage With Gα12.
Article in Transplantation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Extracellular matrix gene set and microRNA network in intestinal ischemia-reperfusion injury: Insights from RNA sequencing for diagnosis and therapy.World journal of gastrointestinal surgery · 2025Review
- GRespiratory research · 2024Review
- Allogeneic bone marrow mesenchymal stem cell-derived exosomes alleviate human hypoxic AKI-on-a-Chip within a tight treatment window.Stem cell research & therapy · 2024Article
- Correlation between the dopaminergic system and inflammation disease: a review.Molecular biology reports · 2023Review
- GαFrontiers in cell and developmental biology · 2022Review
- 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
- Loss of Function in Dopamine D3 Receptor Attenuates Left Ventricular Cardiac Fibroblast Migration and ProliferationFrontiers in cardiovascular medicine · 2021Article
- Newly Developed Dopamine DThe Journal of pharmacology and experimental therapeutics · 2019Article
- Increased renal oxidative stress in salt-sensitive human GRK4γ486V transgenic mice.Free radical biology & medicine · 2017Article
- ICU Management of the Potential Organ Donor: State of the Art.Current neurology and neuroscience reports · 2016Review
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundRenal ischemia-reperfusion (I/R) injury causes renal tubular necrosis, apoptosis, and inflammation leading to acute renal dysfunction. Recent studies have revealed that deletion of Gα12 mitigates the renal damage due to I/R injury. Our previous study showed that activation of dopamine D3 receptor (D3R) increased its linkage with Gα12, and hampered Gα12-mediated stimulation of renal sodium transport. In the present study, we used an in-vivo rat model and an in vitro study of the renal epithelial cell line (NRK52E) to investigate whether or not an increased linkage between D3R and Gα12 contributes to the protective effect of D3R on renal I/R injury.
methodsFor in vivo studies, I/R injury was induced in a rat renal unilateral clamping model. For in vitro studies, hypoxia/reoxygenation and cold storage/rewarming injuries were performed in NRK52E cells. PD128907, a D3R agonist, or vehicle, was administered 15 minutes before clamping (or hypoxia) in both the in vivo or in vitro studies.
resultsIn the rat renal unilateral clamping model, pretreatment with PD128907 (0.2 mg/kg, intravenous) protected against renal I/R injury and increased survival rate during a long-term follow-up after 7 days. A decrease in the generation of reactive oxygen species, apoptosis, and inflammation may be involved in the D3R-mediated protection because pretreatment with PD128907 increased renal glutathione and superoxide dismutase levels and decreased malondialdehyde levels in the I/R group. The increase in cytokines (TNF-α, IL-1β, and IL-10) and myeloperoxidase in I/R injured kidney was also prevented with a simultaneous decrease in the apoptosis of the epithelial cells and expression of apoptosis biomarkers in kidney harvested 1 day after I/R injury. The increase in the coimmunoprecipitation between D3R and Gα12 with D3R stimulation paralleled the observed renal protection from I/R injury. Moreover, in vitro studies showed that transient overexpression of Gα12 in the NRK52E cells attenuated the protective effect of PD128907 on hypoxia/reoxygenation injury. The protective effect of PD128907 might be of significance to renal transplantation because cold storage/rewarming induced injury increased lactate dehydrogenase release and decreased cell viability in NRK52E cells. Conversely, in the presence of PD128907, the increased lactate dehydrogenase release and decreased cell viability were reversed.
conclusionsThese results suggest that activation of D3R, by decreasing Gα12-induced renal damage, may exert a protective effect from I/R injury.
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