Péréon Y, Navarro J, Sorrentino V, Louboutin J P, Noireaud J, Palade P
Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston, TX 77555-0641, USA.
Pflugers Arch. 1997 Jan;433(3):221-9. doi: 10.1007/s004240050271.
One of the the major properties of mature skeletal muscle is its ability to regenerate after injury. The purpose of the present study was to determine whether the expression of genes encoding the dihydropyridine receptor calcium channel (DHPR) and the ryanodine receptor (RyR), which play a critical role in excitation-contraction coupling, is regulated by skeletal muscle regeneration. The process of regeneration was induced by bupivacaine injection in surgically exposed rat extensor digitorum longus (EDL) muscle. After total RNA isolation from the injected and the contralateral control EDL muscles performed 3, 7, 15 and 30 days following injection, Northern blot and RNase protection assays were carried out with four cDNA probes specific for the skeletal and cardiac muscle isoforms of both the DHPR alpha1-subunit and the RyR. After 3 days, an initial precipitous decrease in the expression of the genes encoding the skeletal muscle isoforms of the DHPR and RyR was observed, followed by an increase. Moreover, regenerating skeletal muscle transiently expressed mRNA for the DHPR cardiac isoform, mainly at the beginning of regeneration. No expression of mRNA for the cardiac RyR was observed. Contraction experiments, performed using EDL muscle at the same times after bupivacaine injection, showed that twitch amplitude was markedly decreased in the absence of external calcium, but only during the early stages of regeneration. Similar findings in relation to expression of skeletal and cardiac muscle DHPR message were previously reported from experiments conducted during early developmental stages using fetal skeletal muscle and muscle cell cultures [Chaudhari N, Beam KG (1993) Dev Biol 155:507-515]. These results suggest that expression of the DHPR cardiac isoform in skeletal muscle could explain certain cardiac-like aspects of excitation-contraction coupling of regenerating skeletal muscle and developing skeletal muscle as well.
成熟骨骼肌的主要特性之一是其损伤后再生的能力。本研究的目的是确定在兴奋-收缩偶联中起关键作用的编码二氢吡啶受体钙通道（DHPR）和兰尼碱受体（RyR）的基因表达是否受骨骼肌再生的调节。通过在手术暴露的大鼠趾长伸肌（EDL）中注射布比卡因诱导再生过程。在注射后3、7、15和30天，从注射侧和对侧对照EDL肌肉中分离总RNA后，用针对DHPRα1亚基和RyR的骨骼肌和心肌亚型的四种cDNA探针进行Northern印迹和核糖核酸酶保护分析。3天后，观察到编码DHPR和RyR骨骼肌亚型的基因表达最初急剧下降，随后增加。此外，再生骨骼肌短暂表达DHPR心脏亚型的mRNA，主要在再生开始时。未观察到心脏RyR的mRNA表达。在布比卡因注射后相同时间使用EDL肌肉进行的收缩实验表明，在无细胞外钙的情况下，抽搐幅度明显降低，但仅在再生早期。先前在早期发育阶段使用胎儿骨骼肌和肌肉细胞培养进行的实验中也报道了与骨骼肌和心肌DHPR信息表达相关的类似发现[Chaudhari N，Beam KG（1993）Dev Biol 155：507-515]。这些结果表明，骨骼肌中DHPR心脏亚型的表达可以解释再生骨骼肌和发育中的骨骼肌兴奋-收缩偶联的某些类似心脏的方面。
