Table 1.
Source | Type of endothelial cell | Effect/mechanism | Ref. |
---|---|---|---|
Tumor necrosis factor-alpha (TNF-α) | Human umbilical vein endothelial cells (HUVECs) | (i) Induction of oxidative stress, inflammation, and apoptosis (ii) Induction of inflammation and monocytes adhesion |
[28,29] |
Glycated low-density lipoprotein (glyLDL) | Porcine aortic EC (PAEC) | (i) Induction of oxidative stress and apoptosis | [30] |
Bradykinin | HUVECs | (i) Induction of endothelial hyperpermeability (ii) Stimulation of angiogenesis via increased endothelial permeability and remodeling |
[31,32] |
Histamine | HUVEC Human dermal microvascular endothelial cells (HDMEC) |
(i) Increased endothelial permeability through PLC-NO-cGMP signaling cascade (ii) Induction of endothelial dysfunction by activating Ca2+-mediated RhoA and adherens junctions' tension |
[33,34] |
α-Thrombin | HUVECs | (i) Increased endothelial macromolecular permeability | [35] |
IFNγ | HUVEC | (i) Induction of endothelial hyperpermeability via activation of p38 MAP kinase and actin cytoskeleton alteration | [36] |
IL-1α | Brain microvascular endothelial cells (BECs) | Activation and induction of angiogenic markers in endothelial cells | [37] |
IL-1β | Human glomerular endothelial cell (HRGEC) | Induction of vascular hyperpermeability and upregulation of vascular endothelial-cadherin | [38] |
IL-4 | Human coronary artery endothelial cells (HCAEC) and human pulmonary artery endothelial cells (HPAEC) | Induction of vascular hyperpermeability through Wnt5A signaling | [39] |
Lipopolysaccharide (LPS) | HUVECs HUVECs and human lung microvascular endothelial cells (HMVEC-L) |
(i) Induction of apoptosis, injury, JNK phosphorylation, decreased MCL-1 expression and SOD activity, and increased proinflammatory cytokine production. (ii) Activation of endothelial cells' inflammatory responses |
[40,41] |
Thrombin | Primary human dermal microvascular endothelial cells (HDMECs) Human pulmonary microvascular endothelial cells (HPMVECs) |
(i) Induction of microvessel leakage (ii) Induction of vascular hyperpermeability via dysregulation of vascular endothelial (VE-)cadherin and alteration of small rho GTPases |
[42,43] |
Angiotensin II (Ang II) | HUVECs | Induced vascular endothelial cells' injury and oxidative stress | [44] |
Glucose | Rat aortic endothelial cells (RAOECs) | Induces cyclin D2 upregulation and miR‐98 downregulation | [45] |