LymphedemaV1, Main, Exploration, bibRecord, 005424

Role of COX-2 in lymphangiogenesis and restoration of lymphatic flow in secondary lymphedema

Identifieur interne : 005424 ( Main/Exploration ); précédent : 005423; suivant : 005425

Role of COX-2 in lymphangiogenesis and restoration of lymphatic flow in secondary lymphedema

Auteurs : Shinya Kashiwagi [Japon] ; Kanako Hosono [Japon] ; Tatsunori Suzuki [Japon] ; Akira Takeda [Japon] ; Eiju Uchinuma [Japon] ; Masataka Majima [Japon]

Source :

Laboratory investigation [ 0023-6837 ] ; 2011.

RBID : Pascal:11-0419966

Descripteurs français

Pascal (Inist)
- Lymphoedème, Cyclooxygenase 2, Restauration, Lymphatique, Système lymphatique, Secondaire, Facteur croissance endothélium vasculaire, Biologie clinique, Biotechnologie, Lymphangiogenèse, Récepteur LYVE-1, Facteur de croissance endothéliale vasculaire C.
Wicri :
- topic : Biotechnologie.

English descriptors

KwdEn :
- Biotechnology, Clinical biology, Cyclooxygenase 2, Lymphangiogenesis, Lymphatic, Lymphatic Vessel Endothelial Receptor 1, Lymphatic system, Lymphedema, Restoration, Secondary, Vascular endothelial growth factor C, Vascular endothelium growth factor.

Abstract

The pathophysiology of secondary lymphedema remains poorly understood. To clarify the roles of cyclooxygenase (COX)-2 in enhancement of lymphangiogenesis during secondary lymphedema, we tested a mouse tail model and evaluated the recurrence of lymph flow. To induce lymphedema, a circumferential incision was made in the tail of anesthetized mice to sever the dermal lymphatic vessels. The maximum diameters of the tails were measured weekly. We found that the diameters of the tails around the wounds were markedly increased after surgery, and reached maximum size 2 weeks after wounding in mice without a COX-2 inhibitor, celecoxib (Celecoxib-). Expression of COX-2 in wound granulation tissues was markedly increased 1 week after surgery compared with unwounded naive control mice. In Celecoxib-, recurrence of lymphatic flow in the wound granulation tissues was detected 3 weeks after surgical treatment. In contrast, lymphatic flow was markedly suppressed in mice treated with celecoxib (Celecoxib +). Newly formed lymphatic structures were identified in the granulation tissues formed at wounded lesions in Celecoxib-, whereas those were markedly suppressed in Celecoxib+. Interstitial tissue pressures in the distal areas of the tail wounds were markedly increased in Celecoxib + with reduced expression of vascular endothelial cell growth factor (VEGF)-C. F4/80-positive cells were accumulated to the wound granulation tissues in Celecoxib-, and the accumulation of these cells was suppressed in Celecoxib+. Prostaglandin E₂ (PGE₂) upregulated the expressions of VEGF-A and VEGF-C in cultured macrophages, but not human lymphatic microvascular endothelial cells. The present study therefore suggests that lymphangiogenesis, together with recurrence of lymph flow after surgical induction of lymphedema, is upregulated by COX-2 possibly via generation of PGs.

Affiliations:

Japon

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Le document en format XML

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<term>Lymphatic</term>
<term>Lymphatic Vessel Endothelial Receptor 1</term>
<term>Lymphatic system</term>
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<term>Secondaire</term>
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<front><div type="abstract" xml:lang="en">The pathophysiology of secondary lymphedema remains poorly understood. To clarify the roles of cyclooxygenase (COX)-2 in enhancement of lymphangiogenesis during secondary lymphedema, we tested a mouse tail model and evaluated the recurrence of lymph flow. To induce lymphedema, a circumferential incision was made in the tail of anesthetized mice to sever the dermal lymphatic vessels. The maximum diameters of the tails were measured weekly. We found that the diameters of the tails around the wounds were markedly increased after surgery, and reached maximum size 2 weeks after wounding in mice without a COX-2 inhibitor, celecoxib (Celecoxib-). Expression of COX-2 in wound granulation tissues was markedly increased 1 week after surgery compared with unwounded naive control mice. In Celecoxib-, recurrence of lymphatic flow in the wound granulation tissues was detected 3 weeks after surgical treatment. In contrast, lymphatic flow was markedly suppressed in mice treated with celecoxib (Celecoxib +). Newly formed lymphatic structures were identified in the granulation tissues formed at wounded lesions in Celecoxib-, whereas those were markedly suppressed in Celecoxib+. Interstitial tissue pressures in the distal areas of the tail wounds were markedly increased in Celecoxib + with reduced expression of vascular endothelial cell growth factor (VEGF)-C. F4/80-positive cells were accumulated to the wound granulation tissues in Celecoxib-, and the accumulation of these cells was suppressed in Celecoxib+. Prostaglandin E<sub>2</sub>
 (PGE<sub>2</sub>
) upregulated the expressions of VEGF-A and VEGF-C in cultured macrophages, but not human lymphatic microvascular endothelial cells. The present study therefore suggests that lymphangiogenesis, together with recurrence of lymph flow after surgical induction of lymphedema, is upregulated by COX-2 possibly via generation of PGs.</div>
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Role of COX-2 in lymphangiogenesis and restoration of lymphatic flow in secondary lymphedema

Role of COX-2 in lymphangiogenesis and restoration of lymphatic flow in secondary lymphedema

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri