循环总细胞外囊载荷与与年龄相关的氧化应激和对心血管疾病的易感性有关:微阵列数据的探索性结果
Laura Reck Cechinel1,2, Rachael Ann Batabyal2,3,4, Giana Blume Corssac1,5
1Programa de Pós-Graduação em Ciências Biológicas: Fisiologia, Universidade Federal do Rio Grande do Sul, Porto Alegre 90035-003, RS, Brazil.
Biomedicines
|November 25, 2023
概括
衰老改变了携带微RNA和氧化酶的细胞外囊泡和颗粒 (EVP). 这些老老鼠的变化有助于氧化还原失衡,可能导致心血管衰老和心脏病.
科学领域:
- 老年学和心血管研究.
- 分子生物学和氧化应激机制.
背景情况:
- 老龄化是非传染性疾病的重要危险因素,包括心血管和神经退行性疾病.
- 细胞外囊泡和颗粒 (EVP) 携带微RNA,这可能会影响与年龄相关的疾病和氧化应激.
研究的目的:
- 在流通的EVP总量中调查微RNA配置文件的与年龄相关的变化.
- 评估老鼠和年轻老鼠在循环中的EVP总量中的亲和抗氧化酶活性.
主要方法:
- 从年轻 (3个月大) 和老年 (21个月大) 雄性Wistar大鼠的血中分离出总EVP.
- 孤立EVP的MicroRNA微阵列表达式分析,以识别年龄影响的microRNA及其预测目标.
- 在循环的EVP中测量NADPH氧化酶水平,髓氧化酶活性和催化酶活性.
主要成果:
- 循环EVP中的31个成熟的microRNA因年龄而显著改变.
- 预计这些受年龄影响的microRNAs将准与心血管疾病和氧化应激途径有关的分子.
- 来自老老鼠的EVP表现出NADPH氧化酶和髓氧化酶活性增加,以及降低的催化酶活性,这表明氧化还原稳定性受损.
结论:
- 循环的EVP总量含有负载,包括microRNA和氧化酶,这些负载随着年龄的增长而失调.
- 这些与年龄相关的EVP货物的变化有助于衰老期间的氧化还原失衡.
- 这些发现表明,EVP驱动心血管衰老和随后的心脏病的潜在机制.
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