Suppr超能文献

低剂量⁵⁶Fe 粒子和质子辐射对骨骼肌的不同修饰作用。

Divergent modification of low-dose ⁵⁶Fe-particle and proton radiation on skeletal muscle.

机构信息

a Cardiovascular Division and.

出版信息

Radiat Res. 2013 Nov;180(5):455-64. doi: 10.1667/RR3329.1. Epub 2013 Oct 17.

Abstract

It is unknown whether loss of skeletal muscle mass and function experienced by astronauts during space flight could be augmented by ionizing radiation (IR), such as low-dose high-charge and energy (HZE) particles or low-dose high-energy proton radiation. In the current study adult mice were irradiated whole-body with either a single dose of 15 cGy of 1 GeV/n ⁵⁶Fe-particle or with a 90 cGy proton of 1 GeV/n proton particles. Both ionizing radiation types caused alterations in the skeletal muscle cytoplasmic Ca²⁺ ([Ca²⁺]i) homeostasis. ⁵⁶Fe-particle irradiation also caused a reduction of depolarization-evoked Ca²⁺ release from the sarcoplasmic reticulum (SR). The increase in the [Ca²⁺]i was detected as early as 24 h after ⁵⁶Fe-particle irradiation, while effects of proton irradiation were only evident at 72 h. In both instances [Ca²⁺]i returned to baseline at day 7 after irradiation. All ⁵⁶Fe-particle irradiated samples revealed a significant number of centrally localized nuclei, a histologic manifestation of regenerating muscle, 7 days after irradiation. Neither unirradiated control or proton-irradiated samples exhibited such a phenotype. Protein analysis revealed significant increase in the phosphorylation of Akt, Erk1/2 and rpS6k on day 7 in ⁵⁶Fe-particle irradiated skeletal muscle, but not proton or unirradiated skeletal muscle, suggesting activation of pro-survival signaling. Our findings suggest that a single low-dose ⁵⁶Fe-particle or proton exposure is sufficient to affect Ca²⁺ homeostasis in skeletal muscle. However, only ⁵⁶Fe-particle irradiation led to the appearance of central nuclei and activation of pro-survival pathways, suggesting an ongoing muscle damage/recovery process.

摘要

目前尚不清楚宇航员在太空飞行中经历的骨骼肌质量和功能的丧失是否会因电离辐射(IR)而加剧,例如低剂量高电荷和能量(HZE)粒子或低剂量高能质子辐射。在目前的研究中,成年小鼠接受单次 15 cGy 1 GeV/n ⁵⁶Fe 粒子或 90 cGy 1 GeV/n 质子粒子全身照射。这两种电离辐射类型都会改变骨骼肌细胞质钙离子([Ca²⁺]i)稳态。⁵⁶Fe 粒子照射还导致肌浆网(SR)去极化诱发的 Ca²⁺释放减少。[Ca²⁺]i 的增加早在 ⁵⁶Fe 粒子照射后 24 小时就被检测到,而质子照射的影响仅在 72 小时后才显现出来。在这两种情况下,照射后第 7 天[Ca²⁺]i 恢复到基线。所有接受 ⁵⁶Fe 粒子照射的样本在照射后第 7 天都显示出大量中央定位的核,这是再生肌肉的组织学表现。未照射对照或质子照射的样本均未表现出这种表型。蛋白质分析显示,照射后第 7 天,⁵⁶Fe 粒子照射的骨骼肌中 Akt、Erk1/2 和 rpS6k 的磷酸化显著增加,但质子或未照射的骨骼肌则没有,提示促生存信号的激活。我们的研究结果表明,单次低剂量 ⁵⁶Fe 粒子或质子暴露足以影响骨骼肌的钙稳态。然而,只有 ⁵⁶Fe 粒子照射会导致中央核的出现和促生存途径的激活,这表明肌肉损伤/恢复过程仍在继续。

相似文献

1
Divergent modification of low-dose ⁵⁶Fe-particle and proton radiation on skeletal muscle.
Radiat Res. 2013 Nov;180(5):455-64. doi: 10.1667/RR3329.1. Epub 2013 Oct 17.
2
Cardiovascular risks associated with low dose ionizing particle radiation.
PLoS One. 2014 Oct 22;9(10):e110269. doi: 10.1371/journal.pone.0110269. eCollection 2014.
3
Executive function in rats is impaired by low (20 cGy) doses of 1 GeV/u (56)Fe particles.
Radiat Res. 2012 Oct;178(4):289-94. doi: 10.1667/rr2862.1. Epub 2012 Aug 10.
9
Simulated space radiation sensitizes bone but not muscle to the catabolic effects of mechanical unloading.
PLoS One. 2017 Aug 2;12(8):e0182403. doi: 10.1371/journal.pone.0182403. eCollection 2017.

引用本文的文献

本文引用的文献

2
Alterations of biochemical marker levels and myonuclear numbers in rat skeletal muscle after ischemia-reperfusion.
Mol Cell Biochem. 2013 Jan;373(1-2):11-8. doi: 10.1007/s11010-012-1470-0. Epub 2012 Oct 13.
3
Metabolic remodeling agents show beneficial effects in the dystrophin-deficient mdx mouse model.
Skelet Muscle. 2012 Aug 21;2(1):16. doi: 10.1186/2044-5040-2-16.
4
Mitochondrial dysfunction in skeletal muscle of amyloid precursor protein-overexpressing mice.
J Biol Chem. 2012 Jun 8;287(24):20534-44. doi: 10.1074/jbc.M112.359588. Epub 2012 Apr 19.
5
Trpc1 ion channel modulates phosphatidylinositol 3-kinase/Akt pathway during myoblast differentiation and muscle regeneration.
J Biol Chem. 2012 Apr 27;287(18):14524-34. doi: 10.1074/jbc.M112.341784. Epub 2012 Mar 6.
6
Satellite cells say NO to radiation.
Radiat Res. 2011 May;175(5):561-8. doi: 10.1667/RR2453.1. Epub 2011 Feb 14.
7
Activation of AKT signaling promotes cell growth and survival in α7β1 integrin-mediated alleviation of muscular dystrophy.
Biochim Biophys Acta. 2011 Apr;1812(4):439-46. doi: 10.1016/j.bbadis.2011.01.002. Epub 2011 Jan 7.
9
Prolonged space flight-induced alterations in the structure and function of human skeletal muscle fibres.
J Physiol. 2010 Sep 15;588(Pt 18):3567-92. doi: 10.1113/jphysiol.2010.188508. Epub 2010 Jul 26.
10
Differential oxidative stress gene expression profile in mouse brain after proton exposure.
In Vitro Cell Dev Biol Anim. 2010 Sep;46(8):718-25. doi: 10.1007/s11626-010-9330-2. Epub 2010 Jul 7.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验