In vitro regulation of β-adrenoceptor signaling in the rainbow trout, Oncorhynchus mykiss

被引:10
|
作者
Nickerson, JG [1 ]
Drouin, G [1 ]
Perry, SF [1 ]
Moon, TW [1 ]
机构
[1] Univ Ottawa, Dept Biol, Ottawa, ON K1N 6N5, Canada
关键词
beta-arrestin; beta-receptor kinase; clenbuterol; cortisol; down-regulation; hypoxia; phosphorylation;
D O I
10.1023/B:FISH.0000032723.78349.4e
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We review recent advances in the characterization of the beta-adrenoceptor (AR) system of the trout and present new data on the mechanisms of beta-AR desensitization. Phosphorylation of specific amino acids located in the third intracellular loop and cytoplasmic tail regions triggers beta-AR desensitization. Analysis of trout beta-AR sequences reveals a difference in putative phosphorylation profiles between beta-AR subtypes, this suggests that each subtype (beta(2)-, beta(3a)- and beta(3b)-AR) possesses different sensitivity to desensitization. beta-Adrenoceptor kinase (betaARK) and beta-arrestin play a pivotal role in beta-AR desensitization. The tissue distribution of beta-arrestin and betaARK mRNA in trout is reported for the first time and interestingly, both genes appear to be highly expressed in the trout red blood cell. Previous studies reported loss of beta-AR binding sites in trout red blood cells following prolonged receptor activation. Reduction of beta-AR mRNA levels is reported to contribute to down-regulation of beta-ARs in some species. However, we did not detect a significant change in beta-AR mRNA levels in trout subjected to environmental hypoxia, clenbuterol (a beta-agonist) administration, or cortisol administration; therefore, changes in mRNA levels may not contribute to beta-AR desensitization in trout.
引用
收藏
页码:157 / 171
页数:15
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