Prognostic value of soluble angiopoietin-2 and soluble Tie-2 in Egyptian patients with acute myeloid leukemia

Attia, Mohamed A.; Hazzaa, Sahar M.; Essa, Salwa A.; Seleim, Mahmoud F.

doi:10.5152/tjh.2010.50

Cited by 1 publication

(1 citation statement)

References 22 publications

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“…The former could be caused either by shedding of this receptor by cellular proteases or by an active secretion process, in a similar mechanism to that described for sFlt-1, in which this soluble form of the VEGF-A receptor functions as a decoy receptor, modulating the effects of its ligand ( Kendall et al, 1996 ). Of note, higher sTie2 levels have been previously described in conditions such as acute myocardial infarction ( Wang et al, 2005 ), acute myeloid leukemia ( Attia et al, 2010 ), neuroendocrine tumors ( Melen-Mucha et al, 2012 ) and obesity ( Gozal et al, 2017 ), among other conditions associated with inflammation. Moreover, sVEC levels were lower in COVID-19, in an interesting contrast with sepsis ( Zhang et al, 2010 ), autoimmune disease ( Chen et al, 2014 ) and atherosclerosis ( Soeki et al, 2004 ), in which this mediator was consistently higher in patients compared to healthy individuals.…”

Section: Discussionmentioning

confidence: 96%

Association of Ang/Tie2 pathway mediators with endothelial barrier integrity and disease severity in COVID-19

et al. 2023

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Endothelial barrier (EB) disruption contributes to acute lung injury in COVID-19, and levels of both VEGF-A and Ang-2, which are mediators of EB integrity, have been associated with COVID-19 severity. Here we explored the participation of additional mediators of barrier integrity in this process, as well as the potential of serum from COVID-19 patients to induce EB disruption in cell monolayers. In a cohort from a clinical trial consisting of thirty patients with COVID-19 that required hospital admission due to hypoxia we demonstrate that i) levels of soluble Tie2 were increase, and of soluble VE-cadherin were decreased when compared to healthy individuals; ii) sera from these patients induce barrier disruption in monolayers of endothelial cells; and iii) that the magnitude of this effect is proportional to disease severity and to circulating levels of VEGF-A and Ang-2. Our study confirms and extends previous findings on the pathogenesis of acute lung injury in COVID-19, reinforcing the concept that EB is a relevant component of this disease. Our results pave the way for future studies that can refine our understanding of the pathogenesis of acute lung injury in viral respiratory disorders, and contribute to the identification of new biomarkers and therapeutic targets for these conditions.

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