Table 1.
EV source | Stimulus | EV Function | Reference |
---|---|---|---|
HUVEC | Activated protein C | Anti-coagulant | (Perez-Casal et al. 2005) |
Angiogenic factors | Regulate angiogenesis | (Taraboletti et al. 2002) | |
Angiotensin II receptor 1 autoantibody | Impair endothelial function • Induce ROS increase • Reduce NO synthesis |
(Yang et al. 2014) | |
Complement proteins | Exert prothrombinase activity | (Hamilton et al. 1990) | |
C-reactive protein | Possibly contribute to vascular injury | (Wang et al. 2007) | |
High glucose | Induce oxidative stress in EC and promote platelet/EC interactions | (Terrisse et al. 2010) | |
Hypoxia/ reoxygenation |
Induce oxidative stress and apoptosis in cardiomyocytes | (Zhang, Shang, et al. 2016) | |
IL-1α | Pro-coagulant | (Abid Hussein et al. 2008) | |
PAI-1 | Pro-coagulant | (Brodsky et al. 2002) | |
PAI-1 | Impair endothelial function • Inhibit NO production • Increase pulmonary capillary permeability and induce neutrophil recruitment to the lungs |
(Densmore et al. 2006; Buesing et al. 2011) | |
Shear stress | Not assessed | (Vion, Ramkhelawon, et al. 2013) | |
Spontaneously | • Impair angiogenesis* • Increase apoptosis* *In high EV doses |
(Mezentsev et al. 2005) | |
Spontaneously | Suppress monocyte activation • Reduce NF-kB, TNF-α, and IL-1β • Increase IL-10, TGF-β, and MRC1 |
(Njock et al. 2015) | |
TNF-α | Pro-coagulant | (Combes et al. 1999; Szotowski et al. 2005) | |
TNF-α/ Ionizing radiation | Pro-coagulant | (Szotowski et al. 2007) | |
HUVEC & HDMEC |
Ethanol | Promote angiogenesis | (Lamichhane et al. 2017) |
HMEC-1 | Hypoxia | Mediate extracellular matrix remodeling | (de Jong et al. 2016) |
Thrombin | Not assessed | (Sapet et al. 2006) | |
TNF-α | Induce maturation of plasmacytoid dendritic cells | (Angelot et al. 2009) | |
HLMVEC | Intracellular LPS | Not assessed | (Cheng et al. 2017) |
TNF-α | Pro-inflammatory • NF-kB activation in EC • Induce CXCL-10, IL-6, sICAM-1, C5a, and TNF-α release from EC |
(Liu et al. 2017) | |
TNF-α, H2O2, Cigarette smoke |
Not assessed | (Takahashi et al. 2013) | |
HLMVEC & HPAEC |
Cigarette smoke | Suppress efferocytosis | (Serban et al. 2016) |
Hypoxia, LPS | Promote overproliferation and apoptosis resistance in PASMC |
(Zhao et al. 2017) | |
LPS | Induce lung EC barrier disruption | (Sun et al. 2012) | |
Mechanical stretch | Pro-inflammatory Induce alveolar-capillary barrier disruption and neutrophil recruitment to the lungs |
(Vion, Birukova, et al. 2013; Letsiou et al. 2015) | |
HBMEC | Mechanical stretch | Not assessed | (Andrews et al. 2016) |
HAEC | TNF-α | Pro-inflammatory Induce sICAM-1 release |
(Curtis et al. 2009) |
HCAEC | Serum-starved induced apoptosis | Anti-inflammatory • Reduce TNF-α-induced endothelial ICAM-1 expression and monocyte adhesion to EC Mediate EC repair |
(Jansen et al. 2015; Jansen et al. 2013) |
Human EPC | Spontaneously | Promote angiogenesis | (Deregibus et al. 2007) |
Spontaneously | Anti-apoptotic | (Burger et al. 2015) | |
Spontaneously | Promote angiogenesis | (Zhang, Chen, et al. 2016) | |
Spontaneously | Anti-inflammatory • Reduce LPS-induced HMGB-1 and VCAM-1 in EC |
(Zhou et al. 2018) | |
RMVEC | Spontaneously | Impair endothelial function • Reduce NO levels • Impair vasorelaxation • Increase superoxide production |
(Brodsky et al. 2004) |
MLEC | TNF-α | Pro-inflammatory • NF-kB activation and ICAM-1 upregulation in EC |
(Andrews and Rizzo 2016) |
MAEC | Angiotensin II | Pro-inflammatory • VCAM-1 upregulation and ROS increase in EC • Macrophage adhesion |
(Burger et al. 2011) |
bEnd5 | Cytokine Combo/ LPS |
Pro-inflammatory • VEGF-B upregulation in pericytes |
(Yamamoto et al. 2015) |
Abbreviations: HMEC-1 or HDMEC; Human dermal microvascular EC, HLMVEC; Human lung microvascular EC, HBMEC; human brain microvascular EC, HAEC; Human aortic EC, HPAEC; human pulmonary artery EC, HCAEC; human coronary artery EC, EPC; endothelial progenitor cells, MLEC; mouse lung EC, RMVEC; rat renal microvascular EC, MAEC; mouse aortic EC, bEND5; Mouse brain EC, PASMC; pulmonary artery smooth muscle cells.