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作 者:史丹丹[1] 曹永英[2] 曹标[1] 刘幸卉[1] 术蓉[1] 谷瑞彩 肖将尉 丁茂超[1] 黄涛[1] 郭梦霞[1] 廖华[1]
机构地区:[1]南方医科大学解剖学教研室广东省组织构建与检测重点实验室,广州510515 [2]西北民族大学体育学院,兰州730030
出 处:《免疫学杂志》2016年第9期756-761,共6页Immunological Journal
基 金:国家自然科学基金(81171724;81371924;81572102);广东省科技计划(2012B031800146);广东省自然科学基金自由申请项目(2014A030313276)
摘 要:目的探讨钙调蛋白(Calmodulin,CaM)对急性骨骼肌炎症反应的影响。方法心毒素(Cardiotoxin,CTX)肌内注射,诱导C57BL/6小鼠胫骨前肌(tibialis anterior,TA)急性损伤。肌损伤小鼠腹腔注射钙调蛋白抑制剂R24571或激动剂CALP1。分别检测TA肌组织自身抗原和TLRs表达以及单核/巨噬细胞的肌内浸润程度。结果 CTX注射导致急性肌损伤,TA肌内出现大量的炎性渗出,并伴随肌纤维坏死。损伤肌组织内CaM、自身抗原(Mi-2,HRS和Ku70)以及TLR3表达上调。较之CTX损伤组,CALP1处理导致损伤TA肌内单核/巨噬细胞数量增多,肌内自身抗原和TLR3 mRNA和蛋白水平上调,R24571则减少肌内炎性浸润并下调上述炎性介质。结论 CaM信号参与介导急性骨骼肌炎症反应。The Calcium/Calmodulin(Ca^2+/CaM) signaling has been reported to be essential for immune andinflammatory responses in peripheral tissues and organs. However, whether Ca M signaling interferes with muscleinflammation remains mostly unknown. In this study, we investigated the role of Ca M in acute skeletal muscleinflammation. B6 mice of 6-8-week old were induced acute myoinjury by Cardiotoxin(CTX) injection i.m., and thenintraperitoneally injected with Ca M inhibitor R24571 or CaM agonist CALP1, respectively. Muscle-autoantigens,TLRs, and mononuclear/macrophage cells infiltration were detected post-injury. We observed the increase levels ofCa M, muscle autoantigens(Mi-2, HRS and Ku70) and TLR3, as well as intensive intramuscular infiltration ofinflammatory cells after acute injury, while these indicators gradually reduced over time. We also found enhancedintramuscular infiltration of monocytes/macrophages, up-regulated m RNA and protein levels of muscle autoantigens(Mi-2, HRS and Ku70) and TLR3 in the damaged tibialis anterior muscle(TA) treated with CALP1, comparing tountreated one. In contrast, R24571 decreased the intramuscular infiltration, and down-regulated the m RNA andprotein levels of above inflammatory indicator. Thus, the present findings demonstrate Ca M-signal play a role inmediating acute muscle inflammatory responses.
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