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Vascular permeability--the essentials.

Claesson-Welsh L - Ups. J. Med. Sci. (2015)

Bottom Line: This may result in excessive formation of new, unstable, and hyperpermeable vessels with poor blood flow, which further promotes hypoxia and disease propagation.Thus, there is a strong incentive to learn more about an important aspect of vessel biology in health and disease: the regulation of vessel permeability.The current review aims to summarize current insights into different mechanisms of vascular permeability, its regulatory factors, and the consequences for disease.

View Article: PubMed Central - PubMed

Affiliation: Uppsala University, Department of Immunology, Genetics and Pathology, Rudbeck Laboratory , Uppsala , Sweden.

ABSTRACT
The vasculature, composed of vessels of different morphology and function, distributes blood to all tissues and maintains physiological tissue homeostasis. In pathologies, the vasculature is often affected by, and engaged in, the disease process. This may result in excessive formation of new, unstable, and hyperpermeable vessels with poor blood flow, which further promotes hypoxia and disease propagation. Chronic vessel permeability may also facilitate metastatic spread of cancer. Thus, there is a strong incentive to learn more about an important aspect of vessel biology in health and disease: the regulation of vessel permeability. The current review aims to summarize current insights into different mechanisms of vascular permeability, its regulatory factors, and the consequences for disease.

No MeSH data available.


Related in: MedlinePlus

Opening of adherens junction in molecular extravasation. Panel A outlines schematically how VE-cadherin (VEC) engaged in hemophilic interactions at adherens junctions is regulated by hyperphosphorylation, correlating with internalization and degradation of VE-cadherin. VE-cadherin may also recycle; see text. Panel B shows leaky mouse tracheal vasculature after tail-vein injection of VEGF and fluorescent microspheres (white), followed by whole-mount immunostaining for VE-cadherin (red). VEGF-induced vascular leakiness leads to edema.
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Figure 2: Opening of adherens junction in molecular extravasation. Panel A outlines schematically how VE-cadherin (VEC) engaged in hemophilic interactions at adherens junctions is regulated by hyperphosphorylation, correlating with internalization and degradation of VE-cadherin. VE-cadherin may also recycle; see text. Panel B shows leaky mouse tracheal vasculature after tail-vein injection of VEGF and fluorescent microspheres (white), followed by whole-mount immunostaining for VE-cadherin (red). VEGF-induced vascular leakiness leads to edema.

Mentions: Endothelial cell–cell junctions are organized into adherens and tight junctions. The main component of adherens junctions is vascular endothelial (VE)-cadherin, a transmembrane protein which forms homophilic complexes between endothelial cells (15). Adherens junctions dissolve in response to a number of stimuli, including vascular endothelial growth factors (VEGFs) and inflammatory cytokines such as histamine and bradykinin, to allow extravasation of macromolecules (see below). These stimuli cause VE-cadherin dissolution through a triggering event that may involve hyperphosphorylation of VE-cadherin (Figure 2). VE-cadherin is abundantly phosphorylated also in the basal, unstimulated state, through flow-mediated activation of c-Src, which triggers VE-cadherin phosphorylation directly or indirectly (16). The triggering event causing VE-cadherin internalization remains to be identified, and mechanisms different from a direct phosphorylation of VE-cadherin by c-Src have been suggested (17).


Vascular permeability--the essentials.

Claesson-Welsh L - Ups. J. Med. Sci. (2015)

Opening of adherens junction in molecular extravasation. Panel A outlines schematically how VE-cadherin (VEC) engaged in hemophilic interactions at adherens junctions is regulated by hyperphosphorylation, correlating with internalization and degradation of VE-cadherin. VE-cadherin may also recycle; see text. Panel B shows leaky mouse tracheal vasculature after tail-vein injection of VEGF and fluorescent microspheres (white), followed by whole-mount immunostaining for VE-cadherin (red). VEGF-induced vascular leakiness leads to edema.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4526869&req=5

Figure 2: Opening of adherens junction in molecular extravasation. Panel A outlines schematically how VE-cadherin (VEC) engaged in hemophilic interactions at adherens junctions is regulated by hyperphosphorylation, correlating with internalization and degradation of VE-cadherin. VE-cadherin may also recycle; see text. Panel B shows leaky mouse tracheal vasculature after tail-vein injection of VEGF and fluorescent microspheres (white), followed by whole-mount immunostaining for VE-cadherin (red). VEGF-induced vascular leakiness leads to edema.
Mentions: Endothelial cell–cell junctions are organized into adherens and tight junctions. The main component of adherens junctions is vascular endothelial (VE)-cadherin, a transmembrane protein which forms homophilic complexes between endothelial cells (15). Adherens junctions dissolve in response to a number of stimuli, including vascular endothelial growth factors (VEGFs) and inflammatory cytokines such as histamine and bradykinin, to allow extravasation of macromolecules (see below). These stimuli cause VE-cadherin dissolution through a triggering event that may involve hyperphosphorylation of VE-cadherin (Figure 2). VE-cadherin is abundantly phosphorylated also in the basal, unstimulated state, through flow-mediated activation of c-Src, which triggers VE-cadherin phosphorylation directly or indirectly (16). The triggering event causing VE-cadherin internalization remains to be identified, and mechanisms different from a direct phosphorylation of VE-cadherin by c-Src have been suggested (17).

Bottom Line: This may result in excessive formation of new, unstable, and hyperpermeable vessels with poor blood flow, which further promotes hypoxia and disease propagation.Thus, there is a strong incentive to learn more about an important aspect of vessel biology in health and disease: the regulation of vessel permeability.The current review aims to summarize current insights into different mechanisms of vascular permeability, its regulatory factors, and the consequences for disease.

View Article: PubMed Central - PubMed

Affiliation: Uppsala University, Department of Immunology, Genetics and Pathology, Rudbeck Laboratory , Uppsala , Sweden.

ABSTRACT
The vasculature, composed of vessels of different morphology and function, distributes blood to all tissues and maintains physiological tissue homeostasis. In pathologies, the vasculature is often affected by, and engaged in, the disease process. This may result in excessive formation of new, unstable, and hyperpermeable vessels with poor blood flow, which further promotes hypoxia and disease propagation. Chronic vessel permeability may also facilitate metastatic spread of cancer. Thus, there is a strong incentive to learn more about an important aspect of vessel biology in health and disease: the regulation of vessel permeability. The current review aims to summarize current insights into different mechanisms of vascular permeability, its regulatory factors, and the consequences for disease.

No MeSH data available.


Related in: MedlinePlus