Chinese Journal of Tissue Engineering Research ›› 2015, Vol. 19 ›› Issue (7): 1087-1093.doi: 10.3969/j.issn.2095-4344.2015.07.019
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Zheng Pan-pan, Yu Xin-kai, Zuo Qun, Li Wan-wan, Song Ya-yun
Online:
2015-02-12
Published:
2015-02-12
Contact:
Yu Xin-kai, M.D., Associate professor, Shanghai University of Sport, Shanghai 200438, China
About author:
Zheng Pan-pan, Studying for master’s degree, Shanghai University of Sport, Shanghai 200438, China
Supported by:
the National Natural Science Foundation of China, No. 31171139; the Graduate’s Education Innovation Fund of Shanghai University of Sport, No. yjscx2014038; a grant from Shanghai Key Laboratory for Development and Protection of Human Exercise Capacity (Shanghai University of Sport), Ministry of Education, No. 11DZ2261100
CLC Number:
Zheng Pan-pan, Yu Xin-kai, Zuo Qun, Li Wan-wan, Song Ya-yun . Muscle-specific microRNA-206: research status and prospects[J]. Chinese Journal of Tissue Engineering Research, 2015, 19(7): 1087-1093.
2.1 MicroRNA-206的生物合成和作用机制 2.1.1 MicroRNAs的生物合成 miRNA是一类非编码、内源性的小RNA,长21-25个核苷酸,主要调节基因转录后的表达[1],最初是1993年在线虫中发现——lin-4[2-3]。miRNA具有高度保守性,有研究预测多种miRNA都能在其他种系中找到同源体。在206种脊椎动物的研究中,已经发现了30 000多个成熟miRNA[4]。大量研究表明,骨骼肌的生成发展几乎都需要miRNA参与调控,特别是肌原性的miRNA。 目前,在动物体内miRNA的生物合成过程已经得到了较为详尽的诠释。MiRNA基因主要在RNA聚合酶Ⅱ的作用下转录成较长的初级转录产物pri-miRNA[5],有时 RNA聚合酶Ⅲ也会参与。Pri-miRNA在细胞内RNaseⅢ内切酶(Drose)的作用下加工合成70个碱基的pre-miRNA,pre-miRNA在细胞转运蛋白5(exportin 5)作用下被运输到细胞质。在细胞质中,pre-RNA在RNaseⅢ酶(Dicer)的作用下形成22个核苷酸大小的成熟miRNA。 2.1.2 MicroRNA-206的作用方式和调节机制 miRNA通过与靶基因3’UTR区互补配对,指导miRNA复合体对靶mRNA进行切割或者翻译抑制。miRNA抑制mRNA的翻译机制至今为止还不是很清楚,但能够确定的是,miRNA 5’端2-8个核苷酸对于miRNA与3’UTR的配对非常重要,因此把5’端的这个部位称之为“种子”序列[6-7]。miRNA抑制mRNA的翻译机制至今为止是个迷。目前认为,miRNA对靶基因的作用机制主要有3种:miRNA与靶mRNA 完全互补结合,切割靶mRNA;miRNA与靶mRNA不完全互补结合,抑制靶蛋白翻译而不影响mRNA的稳定性;同时具有以上两种作用模式。动物的miRNA与靶序列的配对性较低,多数是对mRNA进行翻译抑制。 很多miRNA在某些特定的组织里高表达,在骨骼肌内特异性表达的miRNA的叫骨骼肌特异性miRNA,包括miR-1、miR-133a、miR -133b、miR -206、miR-208、miR-208b、miR-486和miR-499等[8-12]。这个亚类miRNA在肌肉组织中特异存在,参与肌肉形成过程中细胞的增殖和分化。MiR-206是骨骼肌特异性miRNA,是2003年从人和小鼠肌肉组织中克隆鉴定出来的,人、小鼠和大鼠的miR-206分别位于第6、1和9号染色体上[13],长度为22个核苷酸,是唯一只在骨骼肌中特异性表达的miRNA[14],在小鼠、鸡和青蛙胚胎发育中miR-206仅限于体节表达[14-15](见图1)。2006年chen等[16]通过基因芯片检测到miR-206在骨骼肌细胞分化成熟过程中表达增加且呈现一定的时空特异性。"
目前已发现多种转录因子能够激活并促进miRNA-206的转录过程。MRFS(生肌调节因子)-比较典型的是MyoD和bHLH,它们能通过调节miRNA-206来控制肌肉发育[17-18]。肌细胞分化因子MyoD能够促进横纹肌特异性miRNA的表达,刺激miR-206的表达能激活骨骼肌分化。Kim等[19]发现miR-206可通过下调MyoD的抑制因子MyoR等上调MyoD基因表达。转化生长因子β能通过抑制miR-206来改变HDAC4的表达[20]。 一个miRNA可以被多个靶基因所调控,同时一个miRNA可以调节多个靶基因。缝隙链接蛋白Cx43是miR-1/miR-206的靶基因[5,19],而Cx43的下调是成肌细胞融合的必要条件[21]。受体酪氨酸激酶(c-Met)是miR-206的靶基因,在横纹肌肉瘤细胞株中被确定,c-Met过度表达的肿瘤中,细胞异常地增殖和迁移,而miR-206能作为一种强有力的肿瘤抑制剂[22-23]。MiR-206另一个靶基因是HDAC4[16,24],是肌肉基因转录表达的抑制位点,HDAC4能部分介导miR-206的功能,在人体神经损伤后能促进神经突触的恢复,延缓肌萎缩侧索硬化症模型老鼠发病的进程[24]。miR-1和miR-206的靶基因Pax7的主要作用是抑制卫星细胞增殖[25-27]。在C2C12成肌细胞系中,miR-206通过DNA聚合酶α来影响mRNA的表达,miR-206的下调会通过抑制DNA的合成从而影响肌细胞的分化。B-ind1和Mnd也是miR-206的靶基因[19]。MiR-206可以通过调节基因-Hmgb3表达和DNA聚合酶的合成,抑制肌细胞的增殖、促进分化[28]。更多的miR-206的靶基因正在被预测和验证,包括卵泡抑素样1(Fstl1)[29],抗肌萎缩相关蛋白(Utrn)[29],和组织型基质金属蛋白酶抑制因子3(TIMP3)[30]。鉴定miRNA的靶基因是研究miRNAs功能发挥的关键,但现在仍是一个技术挑战。 2.2 MicroRNA-206在疾病中的表达 2.2.1 MicroRNA-206在骨骼肌疾病中的表达 研究证实,多种miRNA在心肌和骨骼肌疾病中表达失调,个别miRNA的表达异常可引起或减缓疾病的发生和进展。如在小鼠不同的发展阶段和不同组织进行Dicer的敲除,在胚胎早期Dicer酶缺陷的小鼠,肌肉质量的减少,肌细胞凋亡的增加,伴随着非正常的肌纤维,证明了miRNA在肌肉发育中扮演的关键性角色[31-33]。 杜氏肌营养不良(DMD)的患者体内,miR-223、miR-449和miR-206表达上升。Dystrophin基因缺失的mdx小鼠是研究肌营养不良发病机制和骨骼肌损伤再生机理的常用模型[34-35]。Mccarthy等[9]通过原位杂交显示,miR-206在mdx小鼠的膈膜和再生形成的肌肉中表达上升,而在完整的肌纤维中没有出现,暗示miR-206可能参与了肌肉损伤后的修复过程,提示了miR-206可能在促进肌纤维再生中有重要作用。Liu等[36]研究发现,4周龄mdx老鼠和正常老鼠相比,骨骼肌发生坏死和变性,mdx老鼠体内miR-206水平显著上升,并集中在新生肌管和再生的肌纤维中,而完整的肌纤维中并没有出现[27,37]。这些研究都显示miR-206在骨骼肌损伤再生的病理过程中发挥着重要作用。 强直性肌营养不良1型(DM1)的大部分患者,miR-206表达显著上升。但有趣的是,DM1患者和正常对照组相比,与miRNA-206有关的靶基因、mRNA和抗肌萎缩相关蛋白的水平都没有显著性差异[38]。Liu等[39]对肌营养不良的受试者进行干细胞疗法时发现,低氧水平能激活Notch信号通路,通过Hes/Hey蛋白来抑制miR-206和miR-1的表达,从而增加Pax7的表达,提高干细胞的自我更新和存活能力。 横纹肌肉瘤是一种恶性软组织瘤,由骨骼肌细胞分化程度低导致,现有治疗横纹肌肉瘤的方法具有明显的毒性,寻找一种新的治疗方法来治疗横纹肌肉瘤十分重要。MiR-206的水平和横纹肌肉瘤的临床表现有一定的相关性,横纹肌肉瘤患者骨骼肌内miR-206水平明显比正常人低[13]。MacQuarrie等[40]证实,miR-206能调控细胞从生长向分化转化。同时,Missiaglia等[41]发现miR-206的低表达会激活MAPK和核因子kB信号通路,而miR-206的超表达能通过转变横纹肌肉瘤细胞中总mRNA的表达来促进肌肉的分化,抑制细胞的增殖和迁移。 Williams等[24]证明在神经退行性疾病--肌萎缩侧索硬化症大鼠模型体内miR-206的表达上升,并且发现缺乏miR-206会加重肌萎缩侧索硬化症老鼠的病情,促进神经肌肉突触的变性。MiR-206对肌萎缩侧索硬化症的保护性效应可通过作用于靶位点HDAC4实现,这反过来又刺激FGF信号通路,促进损伤的运动神经元神经肌肉突触代偿性增生,从而减缓肌萎缩侧索硬化症进程[24]。也有研究显示,miR-206在神经肌肉再生过程中表达上升,通过作用于不同的分子,包括脑源性神经营养因子和它的受体(P75NTR)[42],促进肌纤维和运动神经元轴突之间的交流,从而减缓肌萎缩侧索硬化症的病情发展。最近,Valdez等[43]也证明,miR-206能调节神经肌肉损伤后神经肌肉接点的恢复。MiR-206对肌萎缩侧索硬化症的修复作用提示人们,控制miR-206的水平可能成为治疗肌萎缩侧索硬化症的新方法。 2.2.2 MicroRNA-206在其他疾病中的表达 人类很多疾病都与miRNA有密切联系[44]。哺乳类动物的miRNA主要是通过减少目标mRNA的翻译水平来抑制基因的表达,估计超过60%的人类蛋白质的基因编码都要在miRNA的调节下进行[45]。 生理条件下miR-206是骨骼肌特异性miRNA[14],如在正常人大脑内miR-206的表达在一个比较低的水平[46],在健康的心脏中miR-206的水平也几乎检测不到[47]。而在患某些疾病情况下,miR-206的水平会增加,如在心肌梗死、糖尿病型心肌病或者其他心脏疾病的情况下[47]。MiR-206已被认为一种抑癌基因,在肾细胞癌和子宫内腺癌中均发现miR-206表达上调能抑制细胞的增殖和转移[48-49]。 2.3 MicroRNA-206在骨骼肌损伤和运动中的研究 2.3.1 MicroRNA-206在肌肉损伤中的研究 骨骼肌损伤能激活成熟的肌原性干细胞-卫星细胞来进行骨骼肌的再生。骨骼肌损伤早期,卫星细胞中miR-206下调,这种现象是因为早期阶段miR-1和miR-206受到卫星细胞的抗增殖作用[50],pax7水平上升增加卫星细胞的增殖能力,损伤后期,miR-206水平上升,促进卫星细胞的分化和肌管的融合,揭示了miR-206在骨骼肌再生中的重要作用。MiR-206在骨骼肌损伤中的研究(表1)。 "
Mccarthy等[8]通过切除协同肌造成跖肌肥大,作者发现实验组miR-206和pri-206的表达不同步,pri-miR-206是对照组的18.3倍,miR-206表达水平没有显著性改变。提示miR-206可能与骨骼肌功能性肥大有关。因此,后续研究可以检测骨骼肌肥大后期时间点miR-206的表达是否会上升。 众多研究结果显示,骨骼肌严重损伤后miR-206的变化比较明显。Nakasa等[52]用手术刀切割损伤部分大鼠胫骨前肌肌腹,发现大鼠胫骨前肌撕裂7 d内,miR-206表达先下降再上升。他们还发现,给对照组注射siRNA,实验组局部注射相同剂量双链miR-1,miR-133和miR-206的混合物。在注射后的3-7d,发现注射miR-1,miR-133和miR-206的混合物能促进MyoD1、myogenin和 Pax7 mRNA和蛋白质的表达。1周后发现实验肌肉内形态学和生理学功能的再生,纤维化程度也比对照组小。说明外源性的注射miR-1、miR-133和miR-206能诱导肌原性标记物的表达,加速大鼠骨骼肌的再生。同时,在体外培养中发现,加入miR-1,miR-133和miR-206的混合物,能促进肌管的分化,同时MyoD1、myogenin和Pax7的表达上升。这些实验都证明了miR-1,miR-133和miR-206在骨骼肌生长和发育过程中起着至关重要的调节作用。Liu等[36]也发现miR-206的缺乏,会导致卫星细胞延迟分化,miR-206的缺乏会加剧mdx小鼠营养不良的状况,延迟肌肉的再生和成熟。因此,局部注射miR-1,miR-133和miR-206可能成为治疗骨骼肌损伤的新方法。 Roberts等[53]在正常小鼠胫骨前肌注射25 µL 10-5 mol/L的心脏毒素,15 min、4 d、5 d后,虽然小鼠血清中miR-206的水平表达没有显著性差异,但在注射心脏毒素后15 min miR-206的表达有一定的上升趋势。作者认为创伤后的血清取样密度不够频繁,并不能真正代表创伤后血清中miR-206的表达变化状况。研究还发现,胫骨前肌内miR-206及其转录因子的表达和血清中有一定的相关性,暗示了细胞外的miRNA可能成为评测骨骼肌再生状态的指标。 Yuasa等[37]在mdx小鼠胫骨前肌注射CTX造成损伤后,miR-206水平先下降再升高,第5天miR-206的水平是损伤前的10倍。MiR-1和MiR-133a在损伤后先下降再上升,到第4周恢复到注射前水平。同时Yuasa还通过原位杂交发现,miR-206主要集中在新生的肌管、再生的肌肉和不成熟的肌纤维中,而未受损的肌纤维和小单核细胞中没有miR-206的表达,证实了miR-206与肌肉的再生有关。 Liu等[36]做了类似研究,对正常小鼠胫骨前肌注射CTX发现,miR-206的表达也是呈先下降再升高再下降趋势,有趣的是,正常小鼠在30 d时miR-206恢复到了实验前水平,而Yuasa等的mdx小鼠在损伤8周后仍保持在一个较高的水平,进一步支持了miR-206能促进肌肉的再生。 2.3.2 MicroRNA-206在运动中的研究 在体育训练领域,需要新的生物学标记来评价运动量和运动负荷等情况。近年来,众多研究探索了短期和长期运动对miR-206在肌肉和血液中的影响,暗示了miR-206可能成为运动训练、运动损伤等方面的指标。MiR-206在运动中的研究(表2)。 Drummond等[54]对没有训练的男性进行研究,发现青年与老年受试者进行一次抗阻运动3 h和6 h后,青年和老年受试者骨骼肌中pri-miR-206的表达均增加,而miR-206运动前后表达无显著差异。MiR-1的表达水平在青年和老年受试者的骨骼肌中均升高,而miR-133a和miR-206的表达水平均没有变化,其具体机制仍待研究。 长期耐力运动会引起体内miR-206表达的变化。Nielsen等[55]对10名健康男青年进行12周的耐力训练后发现,股外侧肌miR-1、miR-133a、miR-133b和miR-206显著下降,特别是miR-206,减少了49%。这些miRNA的改变在停训后2周回到训练前的水平,而miR-206是如何调节骨骼肌适应耐力运动的机制还不是很清楚。有趣的是,在进行耐力训练前后,分别对受试者进行60 min的65%最大功率的自行车运动,发现运动后即刻、1 h和3 h,miR-206都表达没有显著性差异。这些数据说明miR-206在中等强度生理性刺激之后不会产生变化,但实验不能排除在之后的时间点可能出现的miR-206的变化。 同时,Russell等[56]也做过类似的实验,受试者为9名没有受过训练的健康男子,进行3h的中等强度耐力运动之后,miR-1、miR-133a、miR-133b表达都有上升,而miR-206表达没有变化。接着Russel让受试者经过 10 d的耐力训练后,进行肌肉活检,发现miR-1和miR-31的表达增加,miR-206的表达没有显著性差异。这项实验与Nielsen等[50]的研究相比,不同的地方是运动量和进行长期锻炼持续的时间,这项研究的受试运动量更小,而且锻炼的持续时间比较短,这可能是导致长期运动后两组受试者肌肉miR-206不同变化趋势的原因。 运动后miR-206在血液中的研究在近几年才开始。2008年,有研究首次探索了血液中miRs的改变及其分布情况。之后对血液中miRs水平的变化研究越来越多。Kroh等[60]研究分析了在血清和血浆中miRs分布的差异。Gomes等[58]检测了受试者血液中3种miRNA的变化,发现在半程马拉松后,受试者血浆中的miR-1、miR-133a和miR-206表达上升。Mooren等[59]做了类似的实验,检测了14名男性耐力运动员在马拉松赛后血液中miRs表达的变化。发现血液中miR-499、miR-208、miR-1、miR-133a、miR-206水平在运动后即刻显著性上升,miR-206水平上升幅度最大,运动后即刻大概是运动前的20倍,并且miR-206在运动后24 h变化幅度虽然有所下降,但没有恢复到运动前水平。Aoi等[57]对11名年轻男性进行进行60min70%VO2max的一次性运动,运动后进行测量血清中miR-1、miR-133a、miR-133b、miR-206、miR-208b、miR-486和miR-499的检测,发现只有miR-486一次性运动和长期运动前后有显著性变化,miR-206没有显著性变化。 结合上述研究发现,miR-206在肌肉和血液中的水平对一次性强度不是很大的运动不敏感,但在马拉松比赛这种负荷比较大的运动后水平会显著性上升。miR-206长期运动适应后水平下降,但当运动适应停训一段时间后,miR-206会恢复到原先的水平,而其机制还有待研究。 "
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