Extensive mononuclear infiltration and myogenesis characterize recovery of dysferlin-null skeletal muscle from contraction-induced injuries.
Extensive mononuclear infiltration and myogenesis characterize recovery of dysferlin-null skeletal muscle from contraction-induced injuries.
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广泛的单核浸润和肌生成是无 Dysferlin 骨骼肌从收缩引起的损伤中恢复的特征。
DOI：
10.1152/ajpcell.00122.2009
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Bloch,RobertJ
中科院分区：
文献类型：
--
作者：
Roche,JosephA;Lovering,RichardM;Roche,Renuka;Ru,LisaW;Reed,PatrickW;Bloch,RobertJ
我们研究了dysferlin-null和对照骨骼肌对小鼠踝关节背屈肌大、小应变损伤的反应。我们测量了收缩扭矩，并计数了保留10 kDa荧光素葡聚糖的纤维、坏死纤维、巨噬细胞和具有中央核并表达发育肌球蛋白重链的纤维，以评估收缩功能、膜重新密封、坏死、炎症和肌生成。我们还研究了X射线照射钝化肌生成后的恢复。我们报告说，dysferlin空肌纤维保留10-kDa的葡聚糖大应变损伤后3天，但失去了此后，坏死和炎症。dysferlin无效肌肉的恢复需要肌生成，与对照组相比，其延迟收缩功能的恢复，对照组通过修复受损的肌纤维而从大应变损伤中恢复，而没有显著的炎症、坏死或肌生成。从小应变损伤中恢复控制和dysferlin-null肌肉涉及炎症和坏死，然后是肌生成，所有这些在dysferlin-null肌肉中更明显，恢复更慢。在小应变损伤后，对照和dysferlin-null肌肉也保留了3天的10-kDa葡聚糖。我们的结论是，dysferlin空肌纤维可以生存至少3天的收缩诱导的损伤，但随后被坏死和炎症消除。在dysferlin缺失小鼠中，替代丢失纤维的肌生成似乎没有显著受损。
We studied the response of dysferlin-null and control skeletal muscle to large- and small-strain injuries to the ankle dorsiflexors in mice. We measured contractile torque and counted fibers retaining 10-kDa fluorescein dextran, necrotic fibers, macrophages, and fibers with central nuclei and expressing developmental myosin heavy chain to assess contractile function, membrane resealing, necrosis, inflammation, and myogenesis. We also studied recovery after blunting myogenesis with X-irradiation. We report that dysferlin-null myofibers retain 10-kDa dextran for 3 days after large-strain injury but are lost thereafter, following necrosis and inflammation. Recovery of dysferlin-null muscle requires myogenesis, which delays the return of contractile function compared with controls, which recover from large-strain injury by repairing damaged myofibers without significant inflammation, necrosis, or myogenesis. Recovery of control and dysferlin-null muscles from small-strain injury involved inflammation and necrosis followed by myogenesis, all of which were more pronounced in the dysferlin-null muscles, which recovered more slowly. Both control and dysferlin-null muscles also retained 10-kDa dextran for 3 days after small-strain injury. We conclude that dysferlin-null myofibers can survive contraction-induced injury for at least 3 days but are subsequently eliminated by necrosis and inflammation. Myogenesis to replace lost fibers does not appear to be significantly compromised in dysferlin-null mice.
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