LymphedemaV1, Ncbi, Merge, bibRecord, 008914

Inflammation and Lymphedema Are Exacerbated and Prolonged by Neuropilin 2 Deficiency.

Identifieur interne : 008914 ( Ncbi/Merge ); précédent : 008913; suivant : 008915

Inflammation and Lymphedema Are Exacerbated and Prolonged by Neuropilin 2 Deficiency.

Auteurs : Patrick Mucka [États-Unis] ; Nicholas Levonyak [États-Unis] ; Elena Geretti [États-Unis] ; Bernadette M M. Zwaans [États-Unis] ; Xiaoran Li [États-Unis] ; Irit Adini [États-Unis] ; Michael Klagsbrun [États-Unis] ; Rosalyn M. Adam [États-Unis] ; Diane R. Bielenberg [États-Unis]

Source :

The American journal of pathology [ 1525-2191 ] ; 2016.

RBID : pubmed:27751443

Descripteurs français

English descriptors

KwdEn :
- Animals, Blood Vessels (physiopathology), Capillary Permeability, Female, Humans, Inflammation (genetics), Inflammation (physiopathology), Lymphatic Vessels (physiopathology), Lymphedema (genetics), Lymphedema (physiopathology), Membrane Proteins (genetics), Membrane Proteins (metabolism), Mice, Mice, Inbred BALB C, Nerve Tissue Proteins (genetics), Nerve Tissue Proteins (metabolism), Neuropilin-2 (deficiency), Neuropilin-2 (genetics), Neuropilin-2 (metabolism), Specific Pathogen-Free Organisms, Vascular Endothelial Growth Factor A (genetics), Vascular Endothelial Growth Factor A (metabolism).
MESH :
- chemical , deficiency : Neuropilin-2.
- chemical , genetics : Membrane Proteins, Nerve Tissue Proteins, Neuropilin-2, Vascular Endothelial Growth Factor A.
- genetics : Inflammation, Lymphedema.
- chemical , metabolism : Membrane Proteins, Nerve Tissue Proteins, Neuropilin-2, Vascular Endothelial Growth Factor A.
- physiopathology : Blood Vessels, Inflammation, Lymphatic Vessels, Lymphedema.
- Animals, Capillary Permeability, Female, Humans, Mice, Mice, Inbred BALB C, Specific Pathogen-Free Organisms.

Abstract

The vasculature influences the progression and resolution of tissue inflammation. Capillaries express vascular endothelial growth factor (VEGF) receptors, including neuropilins (NRPs), which regulate interstitial fluid flow. NRP2, a receptor of VEGFA and semaphorin (SEMA) 3F ligands, is expressed in the vascular and lymphatic endothelia. Previous studies have demonstrated that blocking VEGF receptor 2 attenuates VEGFA-induced vascular permeability. The inhibition of NRP2 was hypothesized to decrease vascular permeability as well. Unexpectedly, massive tissue swelling and edema were observed in Nrp2(-/-) mice compared with wild-type littermates after delayed-type hypersensitivity reactions. Vascular permeability was twofold greater in inflamed blood vessels in Nrp2-deficient mice compared to those in Nrp2-intact littermates. The addition of exogenous SEMA3F protein inhibited vascular permeability in Balb/cJ mice, suggesting that the loss of endogenous Sema3F activity in the Nrp2-deficient mice was responsible for the enhanced vessel leakage. Functional lymphatic capillaries are necessary for draining excess fluid after inflammation; however, Nrp2-mutant mice lacked superficial lymphatic capillaries, leading to 2.5-fold greater fluid retention and severe lymphedema after inflammation. In conclusion, Nrp2 deficiency increased blood vessel permeability and decreased lymphatic vessel drainage during inflammation, highlighting the importance of the NRP2/SEMA3F pathway in the modulation of tissue swelling and resolution of postinflammatory edema.

DOI: 10.1016/j.ajpath.2016.07.022
PubMed: 27751443

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Le document en format XML

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<term>Blood Vessels (physiopathology)</term>
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<term>Humans</term>
<term>Inflammation (genetics)</term>
<term>Inflammation (physiopathology)</term>
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<term>Nerve Tissue Proteins (metabolism)</term>
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<term>Vascular Endothelial Growth Factor A (metabolism)</term>
</keywords>
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<term>Facteur de croissance endothéliale vasculaire de type A (génétique)</term>
<term>Facteur de croissance endothéliale vasculaire de type A (métabolisme)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Inflammation (génétique)</term>
<term>Inflammation (physiopathologie)</term>
<term>Lymphoedème (génétique)</term>
<term>Lymphoedème (physiopathologie)</term>
<term>Neuropiline 2 (déficit)</term>
<term>Neuropiline 2 (génétique)</term>
<term>Neuropiline 2 (métabolisme)</term>
<term>Organismes exempts d'organismes pathogènes spécifiques</term>
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<term>Protéines de tissu nerveux (génétique)</term>
<term>Protéines de tissu nerveux (métabolisme)</term>
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<term>Vaisseaux lymphatiques (physiopathologie)</term>
<term>Vaisseaux sanguins (physiopathologie)</term>
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<term>Nerve Tissue Proteins</term>
<term>Neuropilin-2</term>
<term>Vascular Endothelial Growth Factor A</term>
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<term>Lymphedema</term>
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<term>Neuropiline 2</term>
<term>Protéines de tissu nerveux</term>
<term>Protéines membranaires</term>
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<term>Neuropilin-2</term>
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<term>Protéines membranaires</term>
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<term>Vaisseaux lymphatiques</term>
<term>Vaisseaux sanguins</term>
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<term>Lymphedema</term>
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<front><div type="abstract" xml:lang="en">The vasculature influences the progression and resolution of tissue inflammation. Capillaries express vascular endothelial growth factor (VEGF) receptors, including neuropilins (NRPs), which regulate interstitial fluid flow. NRP2, a receptor of VEGFA and semaphorin (SEMA) 3F ligands, is expressed in the vascular and lymphatic endothelia. Previous studies have demonstrated that blocking VEGF receptor 2 attenuates VEGFA-induced vascular permeability. The inhibition of NRP2 was hypothesized to decrease vascular permeability as well. Unexpectedly, massive tissue swelling and edema were observed in Nrp2(-/-) mice compared with wild-type littermates after delayed-type hypersensitivity reactions. Vascular permeability was twofold greater in inflamed blood vessels in Nrp2-deficient mice compared to those in Nrp2-intact littermates. The addition of exogenous SEMA3F protein inhibited vascular permeability in Balb/cJ mice, suggesting that the loss of endogenous Sema3F activity in the Nrp2-deficient mice was responsible for the enhanced vessel leakage. Functional lymphatic capillaries are necessary for draining excess fluid after inflammation; however, Nrp2-mutant mice lacked superficial lymphatic capillaries, leading to 2.5-fold greater fluid retention and severe lymphedema after inflammation. In conclusion, Nrp2 deficiency increased blood vessel permeability and decreased lymphatic vessel drainage during inflammation, highlighting the importance of the NRP2/SEMA3F pathway in the modulation of tissue swelling and resolution of postinflammatory edema.</div>
</front>
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<Abstract><AbstractText>The vasculature influences the progression and resolution of tissue inflammation. Capillaries express vascular endothelial growth factor (VEGF) receptors, including neuropilins (NRPs), which regulate interstitial fluid flow. NRP2, a receptor of VEGFA and semaphorin (SEMA) 3F ligands, is expressed in the vascular and lymphatic endothelia. Previous studies have demonstrated that blocking VEGF receptor 2 attenuates VEGFA-induced vascular permeability. The inhibition of NRP2 was hypothesized to decrease vascular permeability as well. Unexpectedly, massive tissue swelling and edema were observed in Nrp2(-/-) mice compared with wild-type littermates after delayed-type hypersensitivity reactions. Vascular permeability was twofold greater in inflamed blood vessels in Nrp2-deficient mice compared to those in Nrp2-intact littermates. The addition of exogenous SEMA3F protein inhibited vascular permeability in Balb/cJ mice, suggesting that the loss of endogenous Sema3F activity in the Nrp2-deficient mice was responsible for the enhanced vessel leakage. Functional lymphatic capillaries are necessary for draining excess fluid after inflammation; however, Nrp2-mutant mice lacked superficial lymphatic capillaries, leading to 2.5-fold greater fluid retention and severe lymphedema after inflammation. In conclusion, Nrp2 deficiency increased blood vessel permeability and decreased lymphatic vessel drainage during inflammation, highlighting the importance of the NRP2/SEMA3F pathway in the modulation of tissue swelling and resolution of postinflammatory edema.</AbstractText>
<CopyrightInformation>Copyright © 2016 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
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</AffiliationInfo>
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</AffiliationInfo>
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<Initials>E</Initials>
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</AffiliationInfo>
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</AffiliationInfo>
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</AffiliationInfo>
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<Initials>I</Initials>
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   |texte=   Inflammation and Lymphedema Are Exacerbated and Prolonged by Neuropilin 2 Deficiency.
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Inflammation and Lymphedema Are Exacerbated and Prolonged by Neuropilin 2 Deficiency.

Inflammation and Lymphedema Are Exacerbated and Prolonged by Neuropilin 2 Deficiency.

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