ArticleMolecular pharmacology2014
G-protein βγ subunit dimers modulate kidney repair after ischemia-reperfusion injury in rats.
Article in Molecular pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Activation of the cannabinoid receptor 2 increases renal perfusion.Physiological genomics · 2019Article
- Polycystin 1 loss of function is directly linked to an imbalance in G-protein signaling in the kidney.Development (Cambridge, England) · 2018Article
- Selective Cannabinoid 2 Receptor Stimulation Reduces Tubular Epithelial Cell Damage after Renal Ischemia-Reperfusion Injury.The Journal of pharmacology and experimental therapeutics · 2018Article
- Structural and pharmacological basis for the induction of mitochondrial biogenesis by formoterol but not clenbuterol.Scientific reports · 2017Article
- Targeting GPCR-Gβγ-GRK2 signaling as a novel strategy for treating cardiorenal pathologies.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- TRIP13-deficient tubular epithelial cells are susceptible to apoptosis following acute kidney injury.Scientific reports · 2017Article
- Activator of G-protein Signaling 3 Controls Renal Epithelial Cell Survival and ERK5 Activation.Journal of molecular signaling · 2015Article
- Pulmonary preconditioning, injury, and inflammation modulate expression of the candidate tumor suppressor gene ECRG4 in lung.Experimental lung research · 2015Article
- Localization and expression profile of Group I and II Activators of G-protein Signaling in the kidney.Journal of molecular histology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Heterotrimeric G-proteins play a crucial role in the control of renal epithelial cell function during homeostasis and in response to injury. In this report, G-protein βγ subunit (Gβγ) dimer activity was evaluated during the process of tubular repair after renal ischemia-reperfusion injury (IRI) in male Sprague Dawley rats. Rats were treated with a small molecule inhibitor of Gβγ activity, gallein (30 or 100 mg/kg), 1 hour after reperfusion and every 24 hours for 3 additional days. After IRI, renal dysfunction was prolonged after the high-dose gallein treatment in comparison with vehicle treatment during the 7-day recovery period. Renal tubular repair in the outer medulla 7 days after IRI was significantly (P < 0.001) attenuated after treatment with high-dose gallein (100 mg/kg) in comparison with low-dose gallein (30 mg/kg), or the vehicle and fluorescein control groups. Gallein treatment significantly reduced (P < 0.05) the number of proliferating cell nuclear antigen-positive tubular epithelial cells at 24 hours after the ischemia-reperfusion phase in vivo. In vitro application of gallein on normal rat kidney (NRK-52E) proximal tubule cells significantly reduced (P < 0.05) S-phase cell cycle entry compared with vehicle-treated cells as determined by 5'-bromo-2'-deoxyuridine incorporation. Taken together, these data suggest that Gβγ signaling contributes to the maintenance and repair of renal tubular epithelium and may be a novel therapeutic target for the development of drugs to treat acute kidney injury.
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