MiR-106b and MiR-15b Modulate Apoptosis and Angiogenesis in Myocardial Infarction
MiR-106b and MiR-15b Modulate Apoptosis and Angiogenesis in Myocardial Infarction
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MiR-106b 和 MiR-15b 调节心肌梗死中的细胞凋亡和血管生成
DOI：
10.1159/000258197
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发表时间：
2012-01-01
影响因子：
--
通讯作者：
Sun, Xiaobo
中科院分区：
文献类型：
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作者：
Liu, Zhihua;Yang, Dan;Sun, Xiaobo
背景：microRNAs(MiRNAs)被认为是心肌梗死(MI)反应的关键基因调节因子。然而，miRNAs与影响心肌梗死细胞表型的基因靶点之间的总体关系尚未完全阐明。为了更好地了解miRNAs在心肌梗死中的功能作用，我们通过生物信息学技术挖掘了有用的信息。方法：从文献中检索与MI相关的miRNAs，并使用PicTar、TargetScanS和Miranda程序预测其基因靶点。应用基因本体论(GO)和基因靶标的通径分析来揭示miRNAs的功能作用。用Pajek工具对miRNA-基因网络进行了分析。最后，对网络中两个重要的miRNAs进行了验证实验。结果：共检索到119个与MI相关的miRNAs。对其预测基因靶点的GO和通径分析表明，这些失调的miRNAs富含与心血管相关的表型。通过对miRNA-基因网络的研究，揭示了miRNA与基因靶点之间的整体关系，特别是在细胞凋亡和血管生成过程中的作用。此外，实验数据支持生物信息学预测，miR-106b通过抑制p21的表达而作为抗凋亡调节剂，miR-15b显示出抗血管生成的活性。结论：miRNAs在心肌梗死的病理过程中起重要作用。此外，miR-106b和miR-15b可能分别在心肌梗死后的细胞凋亡和血管生成中发挥重要的调节作用。
Background: MicroRNAs (miRNAs) are identified as crucial gene regulators in response to myocardial infarction (MI). However, the overall relationships between miRNAs and the gene targets which contribute to the cellular phenotypes in MI are not fully elucidated. To make a better understanding towards functional roles of miRNAs in MI, useful information was mined through bioinformatic techniques. Method: MI-related miRNAs were retrieved from publications, and PicTar, TargetScanS, and miRanda programs were used to predict their gene targets. Gene ontology (GO) and pathway analyses of gene targets were applied to uncover functional roles of miRNAs. The miRNA-gene networks were illustrated by Pajek tool. Finally, validation experiments were performed towards two important miRNAs in the networks. Result: Up to 119 MI-related miRNAs were retrieved from publications. GO and pathway analyses for their predicted gene targets demonstrated that these dysregulated miRNAs were enriched in cardiovascular-related phenotypes. Through illustrating miRNA-gene networks, overall relationships between miRNAs and gene targets were detected especially in processes of apoptosis and angiogenesis. Moreover, experimental data supported bioinformatic predictions that miR-106b served as an anti-apoptotic modulator through inhibition of p21 expression and miR-15b displayed anti-angiogenesis activity. Conclusion: The miRNAs played essential roles in pathological processes of MI. Further, miR-106b and miR-15b maybe mediated as robust regulators in apoptosis or angiogenesis following MI, respectively.