The angiopoietin-Tie2 signaling axis in the vascular leakage of systemic inflammation

Milam, Katelyn E.; Parikh, Samir M.

doi:10.4161/21688362.2014.957508

Cited by 81 publications

(95 citation statements)

References 82 publications

(112 reference statements)

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“…93 Ang-2 is known to disrupt AJ and can lead to lung injury in mice by mediating the dissociation of Ang-1 from its receptor Tie2 leading to VE-cadherin disruption. 94,95 While murine models of cerebral malaria suggest the Ang-1/-2 axis plays a role in severe disease, 96 analysis of altered Ang-1, Ang-2 and Tie2 protein levels in human brain specimens from adults patients with CM did not discriminate CM from non-CM cases. 97 At present, Ang-2/Ang-1 ratios remain an excellent marker for severe disease, but whether this pathway contributes critically to human cerebral malaria or acute lung injury as seen in sepsis remains unclear.…”

Section: Host Inflammatory Mediatorsmentioning

confidence: 99%

Dynamic interactions ofPlasmodiumspp. with vascular endothelium

Gillrie

2016

Tissue Barriers

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Plasmodial species are protozoan parasites that infect erythrocytes. As such, they are in close contact with microvascular endothelium for most of the life cycle in the mammalian host. The hostparasite interactions of this stage of the infection are responsible for the clinical manifestations of the disease that range from a mild febrile illness to severe and frequently fatal syndromes such as cerebral malaria and multi-organ failure. Plasmodium falciparum, the causative agent of the most severe form of malaria, is particularly predisposed to modulating endothelial function through either direct adhesion to endothelial receptor molecules, or by releasing potent host and parasite products that can stimulate endothelial activation and/or disrupt barrier function. In this review, we provide a critical analysis of the current clinical and laboratory evidence for endothelial dysfunction during severe P. falciparum malaria. Future investigations using state-of-the-art technologies such as mass cytometry and organs-on-chips to further delineate parasite-endothelial cell interactions are also discussed.

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Section: Host Inflammatory Mediatorsmentioning

confidence: 99%

Dynamic interactions ofPlasmodiumspp. with vascular endothelium

Gillrie

2016

Tissue Barriers

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“…Activating mutations in the TIE2 receptor or the downstream signal transducer PIK3CA [p110α catalytic subunit of phosphatidylinositide-3 kinase (PI3K)] cause human venous malformations (VMs) [28–32] while loss-of-function TIE2 mutations result in glaucoma. Increased Ang2 levels are associated with numerous human diseases, including cancer, sepsis, infectious diseases, diabetes, atherosclerosis and tissue injury making the Ang–Tie system an attractive target for the development of future vascular therapies [3,33–35]. Here, we review recent findings highlighting the signalling properties of the Ang–Tie system, its function in vascular development and homeostasis, as well as its contribution to vascular pathologies.…”

Section: Introductionmentioning

confidence: 99%

Angiopoietin–Tie signalling in the cardiovascular and lymphatic systems

Eklund¹,

Kangas²,

2016

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Endothelial cells that form the inner layer of blood and lymphatic vessels are important regulators of vascular functions and centrally involved in the pathogenesis of vascular diseases. In addition to the vascular endothelial growth factor (VEGF) receptor pathway, the angiopoietin (Ang)–Tie system is a second endothelial cell specific ligand–receptor signalling system necessary for embryonic cardiovascular and lymphatic development. The Ang–Tie system also regulates postnatal angiogenesis, vessel remodelling, vascular permeability and inflammation to maintain vascular homoeostasis in adult physiology. This system is implicated in numerous diseases where the vasculature has an important contribution, such as cancer, sepsis, diabetes, atherosclerosis and ocular diseases. Furthermore, mutations in the TIE2 signalling pathway cause defects in vascular morphogenesis, resulting in venous malformations and primary congenital glaucoma. Here, we review recent advances in the understanding of the Ang–Tie signalling system, including cross-talk with the vascular endothelial protein tyrosine phosphatase (VE-PTP) and the integrin cell adhesion receptors, focusing on the Ang–Tie system in vascular development and pathogenesis of vascular diseases.

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“…Studies show that fibrinogen, fibrin and products of fibrinogen degradation can regulate the activity of MMP-2 and VEGF, by activation of PKC and MAPK via the influence of NF-κB. 54,[57][58][59] Several authors have shown an association between CRP and MS levels and indicators of atherosclerotic plaques. Higher plaque scores and greater thickness of the intima and media of vessels have been observed in people with MS.…”

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confidence: 99%

Síndrome metabólica, aterosclerose e inflamação: tríade indissociável?

et al. 2015

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Populations all over the world are increasingly inactive and are consuming increasing quantities of fats and sugars, which is generally linked to industrially processed foods. The consequences have rapidly manifest as an increase in overweight/obesity and in physiological and metabolic changes, such as the Metabolic Syndrome, which is a series of changes in glycemia, lipids and blood pressure. There is evidence of a close relationship between these changes and inflammatory processes, which can also be linked to oxidative stress. These conditions lead to the pathogenesis of vascular abnormalities or intensify metabolic processes that accompany the metabolic syndrome. The objective of this review is to compare the large number of bibliographic references that show correlations between components of the Metabolic Syndrome and increases in the mediators of inflammation. The publications reviewed were located using the Pubmed, Scopus, Lilacs and Scielo databases and the majority of the articles selected were published within the last 5 years.Keywords: metabolic syndrome ; arteriosclerosis; inflammation. ResumoObserva-se, nas populações mundiais, aumento do sedentarismo e aumento do consumo de gorduras e açúcares, sendo estes vinculados normalmente aos alimentos industrializados. A consequência disso rapidamente se manifestou no aumento do sobrepeso/obesidade e na instalação de alterações fisiológicas e metabólicas, como a Síndrome Metabólica, que é representada por alterações na glicemia, nos lipídeos e na pressão arterial. Há evidências de ligação estreita entre estas alterações e os processos inflamatórios, que também podem estar associados ao estresse oxidativo. Estas condições levam à patogênese das alterações vasculares ou intensificam os processos metabólicos que acompanham a Síndrome Metabólica. O objetivo desta revisão foi comparar as inúmeras referências literárias que mostram correlação entre os componentes da Síndrome Metabólica e o aumento dos mediadores de inflamação. Para isso, utilizou-se Pubmed, Scopus, Lilacs e Scielo como base de dados, sendo que os artigos selecionados dataram principalmente dos últimos cinco anos.Palavras-chave: síndrome metabólica; arteriosclerose; inflamação.

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The angiopoietin-Tie2 signaling axis in the vascular leakage of systemic inflammation

Cited by 81 publications

References 82 publications

Dynamic interactions ofPlasmodiumspp. with vascular endothelium

Dynamic interactions ofPlasmodiumspp. with vascular endothelium

Angiopoietin–Tie signalling in the cardiovascular and lymphatic systems

Síndrome metabólica, aterosclerose e inflamação: tríade indissociável?

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