Angiopoietin-1, Angiopoietin-2 and Tie-2 in the Coronary Circulation of Patients With and Without Coronary Collateral Vessels

Vascular Integrity Mediated by Vascular Endothelial Cadherin and Regulated by Sphingosine 1-Phosphate and Angiopoietin-1

“…28,29 Another angiopoietin, Ang2, is thought to compete with Ang1 and induce angiogenesis. 80 Ang1 strengthens the PECAM-1-and VE-cad-mediated intercellular junctions by inducing the dephosphorylation of PECAM-1 and VEcad and by inhibiting TNF-α-induced transmigration of leukocytes. 81 We and others have demonstrated that Ang1 localizes Tie2 to the intercellular junctions by bridging Tie2.…”

Plasma hyaluronan and collateral development in patients with coronary artery disease

“…Several contributing factors have been reported in relation to collateral development such as severity of coronary artery stenosis [3], inflammatory cells [4], and some growth factors like VEGF [5] and angiopoietin [6]. Recent research has highlighted the impact of hyaluronan (also called hyaluronic acid, or hyaluronate, or HA) on vascular permeability through endothelial oligosaccharides, and the importance of HAcell interactions in the cell behavior of arterial endothelial and smooth muscle cells [7,8].…”

Evaluation of oxidized low-density lipoprotein in the coronary circulation of patients with coronary artery disease, and its association with percutaneous coronary intervention

“…Besides, there is no previously published report of depletion of a protein marker during transit by vascular atheroma. However, significant changes in the dynamics of some substances in the coronary circulation, such as endostatin [6] and angiopoietin/tie-2 system [9], have been evidenced by using our same sampling approach. Additionally, it was said that OxLDL, once formed, is transported inside the macrophages of coronary arterial wall that avidly take-up and degrade it leading to foam cell formation [10].…”

“…Details of the coronary procedures were described elsewhere [6]. Coronary artery lesions were characterized by 3 interventional cardiologists according to the American College of Cardiology/American Heart Association lesion classification scheme [7].…”

“…To evaluate the effect of PCI on OxLDL levels within the coronary circulation, we presented the average difference between the sampling locations (VS-minus-CS value, labeled ΔOxLDL) rather than presenting the mean OxLDL in each location. Actually, we adopted this concept in 2 recently published studies [6,9]. Again, there was non-significant difference (post-hoc p = 0.875) of ΔOxLDL between PCI and non-PCI groups ( Table 1).…”