Korajoki Hanna, Vornanen Matti
Department of Biology, University of Eastern Finland, P.O. Box 111, 80101, Joensuu, Finland,
Fish Physiol Biochem. 2014 Apr;40(2):539-49. doi: 10.1007/s10695-013-9864-9. Epub 2013 Sep 19.
The sarcoplasmic reticulum (SR) Ca(2+) release channel or ryanodine receptor (RyR) of the vertebrate heart is regulated by the FK506-binding proteins, FKBP12 and FKBP12.6. This study examines whether temperature-related changes in the SR function of fish hearts are associated with changes in FKBP12 expression. For this purpose, a polyclonal antibody against trout FKBP12 was used to compare FKPB12 expression in cold-acclimated (4 °C, CA) and warm-acclimated (18 °C, WA) rainbow trout (Oncorhynchus mykiss), burbot (Lota lota) and crucian carp (Carassius carassius) hearts. FKBP12 expression was modulated in a species- and tissue-specific manner. Temperature acclimation affected FKBP12 expression only in atrial tissue. Changes in the ventricular FKBP12 expression were not detected in any of the fish species. In the atria of rainbow trout and crucian carp, temperature acclimation produced opposite thermal responses: FKBP12 increased in the trout atrium and decreased in the crucian carp atrium under cold acclimation. In the burbot heart, chronic temperature changes did not affect cardiac FKBP12 levels. Expression of FKBP12 mRNA in rainbow trout and crucian carp hearts suggests that the transcript levels are higher in the ventricle than in the atrium and are elevated by cold acclimation in trout, but not in crucian carp. Since FKBP12 is known to increase the Ca(2+) sensitivity of cardiac RyRs and thereby the opening frequency of the Ca(2+) release channels, temperature-related changes in FKBP12 expression may modify the SR function in excitation-contraction coupling. The cold-induced increase in FKBP12 in the trout atrium and decrease in the crucian carp atrium are consistent with the previously noted increase and decrease, respectively, of SR Ca(2+) stores in cardiac contraction in these species.
脊椎动物心脏的肌浆网（SR）Ca²⁺释放通道或兰尼碱受体（RyR）受FK506结合蛋白FKBP12和FKBP12.6的调节。本研究探讨鱼类心脏SR功能中与温度相关的变化是否与FKBP12表达的变化有关。为此，使用针对鳟鱼FKBP12的多克隆抗体，比较了冷适应（4℃，CA）和热适应（18℃，WA）的虹鳟（Oncorhynchus mykiss）、江鳕（Lota lota）和鲫鱼（Carassius carassius）心脏中FKPB12的表达。FKBP12的表达以物种和组织特异性方式受到调节。温度适应仅影响心房组织中FKBP12的表达。在任何鱼类中均未检测到心室FKBP12表达的变化。在虹鳟和鲫鱼的心房中，温度适应产生了相反的热反应：冷适应时，虹鳟心房中的FKBP12增加，鲫鱼心房中的FKBP12减少。在江鳕心脏中，长期温度变化不影响心脏FKBP12水平。虹鳟和鲫鱼心脏中FKBP12 mRNA的表达表明，转录水平在心室中高于心房，并且在虹鳟中因冷适应而升高，但在鲫鱼中没有。由于已知FKBP12会增加心脏RyRs的Ca²⁺敏感性，从而增加Ca²⁺释放通道的开放频率，因此FKBP12表达中与温度相关的变化可能会改变兴奋-收缩偶联中的SR功能。冷诱导的虹鳟心房中FKBP12增加和鲫鱼心房中FKBP12减少，分别与这些物种心脏收缩中SR Ca²⁺储存量先前观察到的增加和减少一致。
