The Microvasculature as a Participant in Inflammation

Bowden, Jeffrey; McDonald, Donald M.

doi:10.1016/b978-012352325-9/50010-1

Cited by 3 publications

(2 citation statements)

References 259 publications

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“…The inhibitory action of Ang-1 on endothelial gap formation and plasma leakage in the airways has potential clinical significance because mucosal edema is a common feature of inflammatory diseases such as asthma and chronic bronchitis (5,42). Ang-1-like therapeutic agents may be clinically beneficial by reducing airflow obstruction associated with airway edema.…”

Section: Effect Of Ang-1* On Number and Size Of Endothelial Gapsmentioning

confidence: 99%

Angiopoietin-1 decreases plasma leakage by reducing number and size of endothelial gaps in venules

Baffert¹,

Le²,

Thurston³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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129

102

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Section: Effect Of Ang-1* On Number and Size Of Endothelial Gapsmentioning

confidence: 99%

Angiopoietin-1 decreases plasma leakage by reducing number and size of endothelial gaps in venules

Baffert¹,

Le²,

Thurston³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

129

102

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show abstract

“…The increased wall thickness would necessitate an expansion of the microvasculature to accommodate the extra tissue mass, and the abundant, enlarged, and congested mucosal blood vessels contribute to the wall thickness. This vascular contribution is functionally important, because even modest increases in wall thickness can amplify decreases in airway conductance produced by bronchoconstriction (6,(12)(13)(14).…”

Section: Background Of Angiogenesis and Microvascular Remodeling In Amentioning

confidence: 99%

Angiogenesis and Remodeling of Airway Vasculature in Chronic Inflammation

McDonald

2001

Am J Respir Crit Care Med

352

282

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Angiogenesis and microvascular remodeling are known features of chronic inflammatory diseases such as asthma and chronic bronchitis, but the mechanisms and consequences of the changes are just beginning to be elucidated. In a model of chronic airway inflammation produced by Mycoplasma pulmonis infection of the airways of mice or rats, angiogenesis and microvascular remodeling create vessels that mediate leukocyte influx and leak plasma proteins into the airway mucosa. These vascular changes are driven by the immune response to the organisms. Plasma leakage results from gaps between endothelial cells, as well as from increased vascular surface area and probably other changes in the newly formed and remodeled blood vessels. Treatment with long-acting beta2 agonists can reduce but not eliminate the plasma occurring after infection. In addition to the elevated baseline leakage, the remodeled vessels in the airway mucosa are abnormally sensitive to substance P, but not to platelet-activating factor or serotonin, suggesting that the infection leads to a selective upregulation of NK1 receptors on the vasculature. The formation of new vessels and the remodeling of existing vessels are likely to be induced by multiple growth factors, including vascular endothelial growth factor (VEGF) and angiopoietin 1 (Ang1). VEGF increases vascular permeability, but Ang1 has the opposite effect. This feature is consistent with evidence that VEGF and Ang1 play complementary and coordinated roles in vascular growth and remodeling and have powerful effects on vascular function. Regulation of vascular permeability by VEGF and Ang1 may be their most rapid and potent actions in the adult, as these effects can occur independent of their effects on angiogenesis and vascular remodeling. The ability of Ang1 to block plasma leakage without producing angiogenesis may be therapeutically advantageous. Furthermore, because VEGF and Ang1 have additive effects in promoting angiogenesis but opposite effects on vascular permeability, they could be used together to avoid the formation of leaky vessels in therapeutic angiogenesis. Finally, the elucidation of the protective effect of Ang1 on blood vessel leakiness to plasma proteins raises the possibility of a new strategy for reducing airway edema in inflammatory airway diseases such as asthma and chronic bronchitis.

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Angiogenesis in paediatric airway disease

Wilson

Robertson

2002

Paediatric Respiratory Reviews

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The Microvasculature as a Participant in Inflammation

Cited by 3 publications

References 259 publications

Angiopoietin-1 decreases plasma leakage by reducing number and size of endothelial gaps in venules

Angiopoietin-1 decreases plasma leakage by reducing number and size of endothelial gaps in venules

Angiogenesis and Remodeling of Airway Vasculature in Chronic Inflammation

Angiogenesis in paediatric airway disease

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