G protein–coupled receptor kinase 2 modifies the ability of Caenorhabditis elegans to survive oxidative stress |
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Authors: | Stacy A. Henry Selina Crivello Tina M. Nguyen Magdalena Cybulska Ngoc S. Hoang Mary Nguyen Tajinder Badial Nazgol Emami Nasma Awada Johnathen F. Woodward Christopher H. So |
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Affiliation: | 1.Roseman University of Health Sciences School of Pharmacy, 11 Sunset Way, Henderson, NV 89014 USA ;2.Touro University Nevada, Henderson, NV 89014 USA |
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Abstract: | Survival and adaptation to oxidative stress is important for many organisms, and these occur through the activation of many different signaling pathways. In this report, we showed that Caenorhabditis (C.) elegans G protein–coupled receptor kinases modified the ability of the organism to resist oxidative stress. In acute oxidative stress studies using juglone, loss-of-function grk-2 mutants were more resistant to oxidative stress compared with loss-of-function grk-1 mutants and the wild-type N2 animals. This effect was Ce-AKT-1 dependent, suggesting that Ce-GRK2 adjusted C. elegans oxidative stress resistance through the IGF/insulin-like signaling (IIS) pathway. Treating C. elegans with a GRK2 inhibitor, the selective serotonin reuptake inhibitor paroxetine, resulted in increased acute oxidative stress resistance compared with another selective serotonin reuptake inhibitor, fluoxetine. In chronic oxidative stress studies with paraquat, both grk-1 and grk-2 mutants had longer lifespan compared with the wild-type N2 animals in stress. In summary, this research showed the importance of both GRKs, especially GRK2, in modifying oxidative stress resistance. |
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Keywords: | Aging Caenorhabditis elegans (C. elegans) G protein coupled receptor kinase (GRK) Oxidative stress Resistance Stress response |
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