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Oxidative Stress and Mitochondrial Dysfunction in Down's Syndrome: Relevance to Aging and Dementia.唐氏综合征中的氧化应激与线粒体功能障碍：与衰老和痴呆的相关性
Curr Gerontol Geriatr Res. 2012;2012:383170. doi: 10.1155/2012/383170. Epub 2012 Apr 29.
2
Heme oxygenase 1 is induced by miR-155 via reduced BACH1 translation in endothelial cells.血红素加氧酶 1 可通过内皮细胞中 BACH1 翻译减少被 miR-155 诱导。
Free Radic Biol Med. 2011 Dec 1;51(11):2124-31. doi: 10.1016/j.freeradbiomed.2011.09.014. Epub 2011 Sep 17.
3
Down syndrome: national conference on patient registries, research databases, and biobanks.唐氏综合征：患者注册中心、研究数据库和生物库国家会议。
Mol Genet Metab. 2011 Sep-Oct;104(1-2):13-22. doi: 10.1016/j.ymgme.2011.07.005. Epub 2011 Jul 13.
4
Drug-induced cardiac mitochondrial toxicity and protection: from doxorubicin to carvedilol.药物诱导的心脏线粒体毒性与保护：从多柔比星到卡维地洛。
Curr Pharm Des. 2011;17(20):2113-29. doi: 10.2174/138161211796904812.
5
Down syndrome: issues to consider in a national registry, research database and biobank.唐氏综合征：国家注册机构、研究数据库和生物库需要考虑的问题。
Mol Genet Metab. 2011 Sep-Oct;104(1-2):10-2. doi: 10.1016/j.ymgme.2011.03.018. Epub 2011 Mar 26.
6
What's up with down syndrome and leukemia-A lot!唐氏综合征与白血病是怎么回事——关系可大着呢！
Pediatr Blood Cancer. 2011 Jul 15;57(1):1-3. doi: 10.1002/pbc.23033. Epub 2011 Apr 7.
7
Proteomic insights into chronic anthracycline cardiotoxicity.蛋白质组学对慢性蒽环类药物心脏毒性的研究进展。
J Mol Cell Cardiol. 2011 May;50(5):849-62. doi: 10.1016/j.yjmcc.2011.01.018. Epub 2011 Jan 31.
8
Impairment of methyl cycle affects mitochondrial methyl availability and glutathione level in Down's syndrome.甲基循环的损伤会影响唐氏综合征中线粒体甲基的可用性和谷胱甘肽水平。
Mol Genet Metab. 2011 Mar;102(3):378-82. doi: 10.1016/j.ymgme.2010.11.166. Epub 2010 Dec 9.
9
Expression of the anthracycline-metabolizing enzyme carbonyl reductase 1 in hearts from donors with Down syndrome.唐氏综合征供体心脏中蒽环类药物代谢酶羰基还原酶 1 的表达。
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10
Characterization of mitochondrial DNA heteroplasmy using a parallel sequencing system.利用平行测序系统进行线粒体 DNA 异质性分析。
Biotechniques. 2010 Apr;48(4):287-96. doi: 10.2144/000113389.

对患有和未患有唐氏综合征的供体心脏中mtDNA、miR-155和BACH1表达的分析。

Analysis of mtDNA, miR-155 and BACH1 expression in hearts from donors with and without Down syndrome.

作者信息

Hefti Erik, Quiñones-Lombraña Adolfo, Redzematovic Almedina, Hui Jeffrey, Blanco Javier G

机构信息

a Department of Pharmaceutical Sciences, University at Buffalo , The State University of New York , Buffalo , NY , USA.

出版信息

Mitochondrial DNA A DNA Mapp Seq Anal. 2016;27(2):896-903. doi: 10.3109/19401736.2014.926477. Epub 2014 Jun 18.

DOI:10.3109/19401736.2014.926477
PMID:24938108
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4315749/
Abstract

Cancer patients with Down syndrome (DS) are at increased risk for anthracycline-related cardiotoxicity. Mitochondrial DNA (mtDNA) alterations in hearts with-DS may contribute to anthracycline-related cardiotoxicity. Cardiac mtDNA and the mtDNA(4977) deletion were quantitated in samples with- (n = 11) and without-DS (n = 31). Samples with-DS showed 30% lower mtDNA (DS(MT-ND1/18Sratio): 1.48 ± 0.72 versus non-DS(MT-ND1/18Sratio): 2.10 ± 1.59; p = 0.647) and 30% higher frequency of the mtDNA(4977) deletion (DS(% frequency mtDNA(4977)) deletion: 0.0086 ± 0.0166 versus non-DS(% frequency mtDNA(4977)) deletion: 0.0066 ± 0.0124, p = 0.514) than samples without-DS. The BACH1 and microRNA-155 (miR-155) genes are located in chromosome 21, and their products have demonstrated roles during oxidative stress. BACH1 and miR-155 expression did not differ in hearts with- and without-DS. An association between BACH1 and miR-155 expression was detected in hearts without-DS, suggesting alterations between BACH1-miR-155 interactions in the DS settings.

摘要

患有唐氏综合征（DS）的癌症患者发生蒽环类药物相关心脏毒性的风险增加。患有DS的心脏中的线粒体DNA（mtDNA）改变可能导致蒽环类药物相关心脏毒性。对有DS（n = 11）和无DS（n = 31）的样本中的心脏mtDNA和mtDNA（4977）缺失进行了定量分析。有DS的样本显示mtDNA含量低30%（DS（MT-ND1/18S比率）：1.48±0.72，而无DS（MT-ND1/18S比率）：2.10±1.59；p = 0.647），mtDNA（4977）缺失频率高30%（DS（mtDNA（4977）缺失频率%）：0.0086±0.0166，而无DS（mtDNA（4977）缺失频率%）：0.0066±0.0124，p = 0.514）。BACH1和微小RNA-155（miR-155）基因位于21号染色体上，其产物在氧化应激过程中发挥了作用。有DS和无DS的心脏中BACH1和miR-155的表达没有差异。在无DS的心脏中检测到BACH1和miR-155表达之间存在关联，这表明在DS情况下BACH1-miR-155相互作用发生了改变。