余细勇教授发现成体心脏前体细胞外泌体的心肌保护新机制

Johnny · 发表于 2016-6-27 20:47:16

本帖最后由 Johnny 于 2016-6-27 20:52 编辑

广州医科大学余细勇教授发现成体心脏前体细胞来源外泌体的心肌保护新机制

从成年心脏来源的心脏前体细胞已成为心脏保护和修复最有希望的干细胞类型之一。外泌体可在细胞与细胞之间转运细胞来源的蛋白质和核酸，包括各种miRNAs。最新一期的Cell death & disease发表了来自广州医科大学药学院院长/广东省人民医院医学研究中心主任余细勇教授的最新工作。该工作发现了心脏前体细胞（CPC）来源的外泌体miRNAs在氧化应激下保护心肌细胞的新机制。从Sca1(+)CPCs条件培养基中提取外泌体，用免疫印迹检测CD63、CD9和Alix等外泌体标志物，并利用纳米颗粒分析（NTA）和透射电子显微镜进行鉴定。外泌体NTA的测定结果表明，氧化应激诱导的CPCs与正常条件相比分泌更多的外泌体。尽管6个细胞凋亡相关的miRNAs可在两个不同处理的外泌体中检测到，但与正常外泌体进行比较只有miR-21在氧化应激诱导的外泌体中显著上调。同样的氧化应激会导致H9C2心肌细胞miR-21低表达和剪切caspase-3的高表达。但过表达miR-21 mimic后，剪切的caspase-3显著下调。此外，miR-21的mimic或抑制剂的转染和荧光素酶的活性测定证实，程序性细胞死亡4蛋白（PDCD4）是miR-21的靶基因，miR-21/PDCD4在H9C2细胞的抗凋亡作用中起重要作用。 Western印迹和Annexin V/PI结果表明外泌体预处理H9C2后miR-21含量升高，而PDCD4降低，并且与非处理的细胞进行比较，其对氧化应激引起的细胞凋亡具有更好的抵抗能力。这些研究结果表明，CPC来源的外泌体的miR-21通过下调PDCD4发挥抑制凋亡的作用。使用CPC来源的外泌体恢复miR-21/PDCD4信号通路可保护心肌细胞免受氧化应激损伤。因此，外泌体可以作为缺血性心脏疾病的新的治疗手段。

参考文献：

Xiao, J., et al. (2016). "Cardiac progenitor cell-derived exosomes prevent cardiomyocytes apoptosis through exosomal miR-21 by targeting PDCD4." Cell Death Dis 7(6): e2277.

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余细勇教授发表的其他外泌体相关文献：

Feng, Y., et al. (2014). "Heat shock improves Sca-1+ stem cell survival and directs ischemic cardiomyocytes toward a prosurvival phenotype via exosomal transfer: a critical role for HSF1/miR-34a/HSP70 pathway." Stem Cells 32(2): 462-472.

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Feng, Y., et al. (2014). "Ischemic Preconditioning Potentiates the Protective Effect of Stem Cells through Secretion of Exosomes by Targeting Mecp2 via miR-22." PLoS One 9(2): e88685.

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Li, Y., et al. (2015). "Transport of microRNAs via exosomes." Nat Rev Cardiol.

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Liu, J., et al. (2014). "Increased exosomal microRNA-21 and microRNA-146a levels in the cervicovaginal lavage specimens of patients with cervical cancer." Int J Mol Sci 15(1): 758-773.

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