4.7 Article

Intercellular transfer of miR-200c-3p impairs the angiogenic capacity of cardiac endothelial cells

期刊

MOLECULAR THERAPY
卷 30, 期 6, 页码 2257-2273

出版社

CELL PRESS
DOI: 10.1016/j.ymthe.2022.03.002

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资金

  1. Netherlands CardioVascular Research Initiative: the Dutch Heart Foundation
  2. Dutch Federation of University Medical Centers, ZonMw
  3. Royal Netherlands Academy of Sciences
  4. ERC Consolidator Grant [311549 CALMIRS]
  5. VICI Award from NWO [918-156-47]
  6. Dutch CardioVascular Alliance (DCVA)
  7. Impulse Grant 2018 [2012-08, 2014-11]
  8. Dutch Heart Foundation grant [NHS2015T066]
  9. Foundation for Science and Technology of Portugal (FCT) [POCI-01-0145-FEDER-030985, SFRH/BD/111799/2015, SFRH/BD/129317/2017]
  10. H2020 Twinning project RESETageing [GA 952266]
  11. Fundação para a Ciência e a Tecnologia [SFRH/BD/111799/2015, SFRH/BD/129317/2017] Funding Source: FCT

向作者/读者索取更多资源

miR-200c-3p in extracellular vesicles secreted by cardiac myocytes plays a crucial role in the communication between cardiac cells and endothelial cells, affecting cardiac function and disease development.
As mediators of intercellular communication, extracellular vesicles containing molecular cargo, such as microRNAs, are secreted by cells and taken up by recipient cells to influence their cellular phenotype and function. Here we report that cardiac stress-induced differential microRNA content, with miR200c-3p being one of the most enriched, in cardiomyocytederived extracellular vesicles mediates functional cross-talk with endothelial cells. Silencing of miR-200c-3p in mice subjected to chronic increased cardiac pressure overload resulted in attenuated hypertrophy, smaller fibrotic areas, higher capillary density, and preserved cardiac ejection fraction. We were able to maximally rescue microvascular and cardiac function with very low doses of antagomir, which specifically silences miR-200c-3p expression in non-myocyte cells. Our results to cardiac endothelial cells, underlining the importance of cardiac intercellular communication in the pathophysiology of heart failure.

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