Vitamin D Increases Cellular Turnover and Functionally Restores the Skeletal Muscle after Crush Injury in Rats

被引:71
作者
Stratos, Ioannis [1 ,2 ]
Li, Zhengdong [1 ]
Herlyn, Philipp [1 ]
Rotter, Robert [1 ]
Behrendt, Ann-Kathrin [1 ]
Mittlmeier, Thomas [2 ]
Vollmar, Brigitte [1 ]
机构
[1] Univ Rostock, Inst Expt Surg, D-18057 Rostock, Germany
[2] Univ Rostock, Dept Trauma & Reconstruct Surg, D-18057 Rostock, Germany
关键词
D-RECEPTOR; PROLYL; 4-HYDROXYLASE; TISSUE REGENERATION; D SUPPLEMENTATION; ADOLESCENT GIRLS; GROWTH-FACTOR; STEM-CELLS; EXPRESSION; REPAIR; PROLIFERATION;
D O I
10.1016/j.ajpath.2012.11.006
中图分类号
R36 [病理学];
学科分类号
100103 [病原生物学];
摘要
Insufficient skeletal muscle regeneration after injury often impedes the healing process and is accompanied by functional deficiencies or pain. The aim of our study was to provide evidence that vitamin D improves muscle healing after muscle injury. Therefore, we used male rats and induced an injury of the soLeus muscle. After crush injury, animals received either 8.3 mg/kg (332,000 IU/kg) body weight vitamin D or vehicle solution, s.c. After assessment of muscle force at days 1, 4, 14, and 42 after injury, sampling of muscle tissue served for analysis of proliferation, apoptosis, satellite cells, and prolyl-4-hydroxylase-beta expression. Vitamin D application caused a significant increase in cell proliferation and a significant inhibition of apoptosis at day 4 after injury compared to control animals. The numbers of satellite cells were not influenced by the vitamin D application, but there was an increase in proly1.-4-hydroxylase-beta expression, indicative of increased extracellular matrix proteins. This cellular turnover resulted in a faster recovery of contraction forces at day 42 in the vitamin D group. Current data support the hypothesis that vitamin D promotes the regenerative process in injured muscle. Thus, vitamin D treatment may represent a promising therapy to optimize recovery after injury. (Am 3 Pathol 2013, 182: 895-904; http://dx.doi.org/10.1016/j.ajpath.2012.11.006)
引用
收藏
页码:895 / 904
页数:10
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