Maixent J M, Fares M, François C, Delmotte A, Rigoard P
Université du Sud Toulon—Var Équipe de Biologie Moléculaire Marine, PROTÉE La Garde France mmaixent@gmail.com.
Université de Poitiers & CHU la Miléterie NSERM U927, Faculté de Médecine Poitiers France.
Cell Mol Biol (Noisy-le-grand). 2014 Nov 16;60(4):22-9.
Spinal cord injuries (SCI) induce a loss of skeletal muscle mass and functional capacity. The muscle excitability and contractility depend on the plasma membrane potential, regulated by transmembrane ion gradients, and thus necessarily on the Na⁺,K⁺-ATPase activity. The aim of this work was to evaluate the consequences of a spinal cord transection (SCT) on the skeletal muscle Na⁺,K⁺-ATPase and the impact of collateral GlyceroPhosphoLipids enriched in DocosaHexaenoic Acid (GPL-DHA) administration. The Na⁺,K⁺-ATPase activity and membrane expression of Na⁺,K⁺-ATPase α1, α2 and β1 isoforms were assessed by K⁺-stimulated paranitrophenyl phosphatase (pNPPase) measurements and Western Blotting, respectively. The results show that spinal cord transection increased significantly (p<0.05) Na⁺,K⁺-ATPase activity in muscle by 25% and decreased the amounts of α1 isoform and α2 isoform expressions by 50% (p<0.05) respectively compared to controls. The results also show that early injection of GPL-DHA after SCT decreases in membrane skeletal muscle the α1 and α2 isoforms expression but increases the membrane Na⁺,K⁺-ATPase activity. This treament partially restores the membrane expression of the β1 subunit of the Na⁺,K⁺-ATPase. These data suggest that the increase of β1 subunit expression is probably the main trigger to the membrane Na⁺,K⁺-ATPase activation following a trans-synaptic denervation.
脊髓损伤（SCI）会导致骨骼肌质量和功能能力丧失。肌肉的兴奋性和收缩性取决于质膜电位，而质膜电位由跨膜离子梯度调节，因此必然依赖于Na⁺,K⁺-ATP酶活性。本研究的目的是评估脊髓横断（SCT）对骨骼肌Na⁺,K⁺-ATP酶的影响，以及富含二十二碳六烯酸的甘油磷脂（GPL-DHA）辅助给药的作用。分别通过K⁺刺激的对硝基苯磷酸酶（pNPPase）测定和蛋白质免疫印迹法评估Na⁺,K⁺-ATP酶活性以及Na⁺,K⁺-ATP酶α1、α2和β1亚型的膜表达。结果显示，与对照组相比，脊髓横断使肌肉中的Na⁺,K⁺-ATP酶活性显著增加（p<0.05）25%，α1亚型和α2亚型的表达量分别降低50%（p<0.05）。结果还表明，SCT后早期注射GPL-DHA可降低膜骨骼肌中α1和α2亚型的表达，但增加膜Na⁺,K⁺-ATP酶活性。这种治疗部分恢复了Na⁺,K⁺-ATP酶β1亚基的膜表达。这些数据表明，β1亚基表达的增加可能是经突触去神经支配后膜Na⁺,K⁺-ATP酶激活的主要触发因素。
