缺氧心肌细胞来源的外泌体通过miR-208a/b调控心肌成纤维细胞活化、凋亡、迁移和铁下垂。

IF 1.3 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY General physiology and biophysics Pub Date : 2023-03-01 DOI:10.4149/gpb_2022061
Ying Guo, Zi-Dong Bie, Xi Li
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引用次数: 1

摘要

研究发现,心肌细胞和心脏成纤维细胞(cardiac fibroblasts, CFs)可以通过外泌体相互通讯,从而影响彼此的生物学功能,但其机制研究较少。miR-208a/b在心脏中特异性表达,在各种心肌疾病衍生的外泌体中高度表达。缺氧诱导心肌细胞分泌高表达miR-208a/b的外泌体(H-Exo)。将H-Exo加入到CFs共培养中,发现CFs占用外泌体,从而上调miR-208a/b的表达。H-Exo显著促进CFs的活力和迁移,增强α-SMA、I型胶原和III型胶原的表达,促进I型胶原和III型胶原的分泌。miR-208a或/和miR-208b抑制剂显著减弱H-Exo对CF生物学功能的影响。miR-208a/b抑制剂显著提高了CFs的凋亡水平和caspase-3活性,而H-Exo显著减弱了miR-208a/b抑制剂的促凋亡作用。用铁下垂诱导剂Erastin进一步处理CFs发现,H-Exo进一步增强了铁下垂主要指标ROS、MDA和Fe2+的积累,抑制了铁下垂关键调控因子GPX4的表达。miR-208a或/和miR-208b抑制剂显著减弱Erastin和H-Exo对铁下垂的影响。综上所述,缺氧心肌细胞来源的外泌体可以通过高表达的miR-208a/b调节CFs的生物学功能。
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Hypoxic cardiomyocyte-derived exosomes regulate cardiac fibroblast activation, apoptosis, migration and ferroptosis through miR-208a/b.

Studies have found that cardiomyocytes and cardiac fibroblasts (CFs) can communicate through exosomes, thereby affecting each other's biological functions, but there are few studies on the mechanism. miR-208a/b are specifically expressed in the heart and highly expressed in exosomes derived from various myocardial diseases. Hypoxia induced cardiomyocytes to secrete exosomes (H-Exo) with high expression of miR-208a/b. When H-Exo were added to CFs for co-culture, it was found that CFs took up exosomes, thereby upregulating the expression of miR-208a/b. H-Exo significantly promoted the viability and migration of CFs, enhanced the expression of α-SMA, collagen I and III, and promoted the secretion of collagen I and III. miR-208a or/and miR-208b inhibitors significantly attenuated the effects of H-Exo on CF biological functions. miR-208a/b inhibitors significantly enhanced the levels of apoptosis and caspase-3 activity in CFs, while H-Exo significantly attenuated the pro-apoptotic effects of miR-208a/b inhibitors. Further treatment of CFs with ferroptosis inducer Erastin found that H-Exo further enhanced the accumulation of ROS, MDA and Fe2+, the main indicators of ferroptosis, and inhibited the expression of GPX4, a key regulator of ferroptosis. miR-208a or/and miR-208b inhibitors significantly attenuated the effects of Erastin and H-Exo on ferroptosis. In conclusion, hypoxic cardiomyocyte-derived exosomes can regulate the biological functions of CFs through highly expressed miR-208a/b.

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来源期刊
General physiology and biophysics
General physiology and biophysics 生物-生化与分子生物学
CiteScore
2.70
自引率
0.00%
发文量
42
审稿时长
6-12 weeks
期刊介绍: General Physiology and Biophysics is devoted to the publication of original research papers concerned with general physiology, biophysics and biochemistry at the cellular and molecular level and is published quarterly by the Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences.
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