TY - JOUR
T1 - Extracellular Vesicle miRNAs in the Promotion of Cardiac Neovascularisation
AU - Kesidou, Despoina
AU - Martins, Paula A. da Costa
AU - de Windt, Leon J.
AU - Brittan, Mairi
AU - Beqqali, Abdelaziz
AU - Baker, Andrew Howard
N1 - Funding Information:
DK was funded by a Ph.D. studentship from Medical Research Scotland. AB was supported by European Union Horizon 2020 CardioReGenix Grant no. 825670. AHB was supported by the British Heart Foundation Chair of Translational Cardiovascular Sciences and European Research Council Advanced Grant VASCMIR and Horizon 2020 grant CARDIOREGENIX. MB was supported by a British Heart Foundation Intermediate Basic Science Research Fellowship (FS/16/4/31831) and by the BHF Centre for Vascular Regeneration (RM/17/3/33381). PdC was supported by a Dutch Heart Foundation grant (NHS2015T066).
Publisher Copyright:
© Copyright © 2020 Kesidou, da Costa Martins, de Windt, Brittan, Beqqali and Baker.
PY - 2020/9/25
Y1 - 2020/9/25
N2 - Cardiovascular disease (CVD) is the leading cause of mortality worldwide claiming almost 17. 9 million deaths annually. A primary cause is atherosclerosis within the coronary arteries, which restricts blood flow to the heart muscle resulting in myocardial infarction (MI) and cardiac cell death. Despite substantial progress in the management of coronary heart disease (CHD), there is still a significant number of patients developing chronic heart failure post-MI. Recent research has been focused on promoting neovascularisation post-MI with the ultimate goal being to reduce the extent of injury and improve function in the failing myocardium. Cardiac cell transplantation studies in pre-clinical models have shown improvement in cardiac function; nonetheless, poor retention of the cells has indicated a paracrine mechanism for the observed improvement. Cell communication in a paracrine manner is controlled by various mechanisms, including extracellular vesicles (EVs). EVs have emerged as novel regulators of intercellular communication, by transferring molecules able to influence molecular pathways in the recipient cell. Several studies have demonstrated the ability of EVs to stimulate angiogenesis by transferring microRNA (miRNA, miR) molecules to endothelial cells (ECs). In this review, we describe the process of neovascularisation and current developments in modulating neovascularisation in the heart using miRNAs and EV-bound miRNAs. Furthermore, we critically evaluate methods used in cell culture, EV isolation and administration.
AB - Cardiovascular disease (CVD) is the leading cause of mortality worldwide claiming almost 17. 9 million deaths annually. A primary cause is atherosclerosis within the coronary arteries, which restricts blood flow to the heart muscle resulting in myocardial infarction (MI) and cardiac cell death. Despite substantial progress in the management of coronary heart disease (CHD), there is still a significant number of patients developing chronic heart failure post-MI. Recent research has been focused on promoting neovascularisation post-MI with the ultimate goal being to reduce the extent of injury and improve function in the failing myocardium. Cardiac cell transplantation studies in pre-clinical models have shown improvement in cardiac function; nonetheless, poor retention of the cells has indicated a paracrine mechanism for the observed improvement. Cell communication in a paracrine manner is controlled by various mechanisms, including extracellular vesicles (EVs). EVs have emerged as novel regulators of intercellular communication, by transferring molecules able to influence molecular pathways in the recipient cell. Several studies have demonstrated the ability of EVs to stimulate angiogenesis by transferring microRNA (miRNA, miR) molecules to endothelial cells (ECs). In this review, we describe the process of neovascularisation and current developments in modulating neovascularisation in the heart using miRNAs and EV-bound miRNAs. Furthermore, we critically evaluate methods used in cell culture, EV isolation and administration.
KW - ANGIOGENIC PROPERTIES
KW - ENDOTHELIAL PROGENITOR CELLS
KW - EXOSOMES
KW - GOVERNS VASCULAR INTEGRITY
KW - HEART-FAILURE PATIENTS
KW - INDUCE ANGIOGENESIS
KW - INHIBITS ANGIOGENESIS
KW - MICRORNA BIOGENESIS
KW - MYOCARDIAL-INFARCTION
KW - PARACRINE MECHANISMS
KW - angiogenesis
KW - cardiac
KW - exosome (EXO)
KW - extracellular vesicles (EV)
KW - microRNA (miR)
KW - myocardial infarct
KW - neovascularisation
KW - regeneration
U2 - 10.3389/fphys.2020.579892
DO - 10.3389/fphys.2020.579892
M3 - (Systematic) Review article
C2 - 33101061
SN - 1664-042X
VL - 11
JO - Frontiers in physiology
JF - Frontiers in physiology
M1 - 579892
ER -