Nitric oxide permits hypoxia-induced lymphatic perfusion by controlling arterial-lymphatic conduits in zebrafish and glass catfish

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Standard

Nitric oxide permits hypoxia-induced lymphatic perfusion by controlling arterial-lymphatic conduits in zebrafish and glass catfish. / Dahl Ejby Jensen, Lasse; Cao, Renhai; Hedlund, Eva-Maria; Söll, Iris; Lundberg, Jon O; Hauptmann, Giselbert; Steffensen, John Fleng; Cao, Yihai.

I: Proceedings of the National Academy of Science of the United States of America, Bind 106, Nr. 43, 2009, s. 18408-13.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Dahl Ejby Jensen, L, Cao, R, Hedlund, E-M, Söll, I, Lundberg, JO, Hauptmann, G, Steffensen, JF & Cao, Y 2009, 'Nitric oxide permits hypoxia-induced lymphatic perfusion by controlling arterial-lymphatic conduits in zebrafish and glass catfish', Proceedings of the National Academy of Science of the United States of America, bind 106, nr. 43, s. 18408-13. https://doi.org/10.1073/pnas.0907608106

APA

Dahl Ejby Jensen, L., Cao, R., Hedlund, E-M., Söll, I., Lundberg, J. O., Hauptmann, G., Steffensen, J. F., & Cao, Y. (2009). Nitric oxide permits hypoxia-induced lymphatic perfusion by controlling arterial-lymphatic conduits in zebrafish and glass catfish. Proceedings of the National Academy of Science of the United States of America, 106(43), 18408-13. https://doi.org/10.1073/pnas.0907608106

Vancouver

Dahl Ejby Jensen L, Cao R, Hedlund E-M, Söll I, Lundberg JO, Hauptmann G o.a. Nitric oxide permits hypoxia-induced lymphatic perfusion by controlling arterial-lymphatic conduits in zebrafish and glass catfish. Proceedings of the National Academy of Science of the United States of America. 2009;106(43):18408-13. https://doi.org/10.1073/pnas.0907608106

Author

Dahl Ejby Jensen, Lasse ; Cao, Renhai ; Hedlund, Eva-Maria ; Söll, Iris ; Lundberg, Jon O ; Hauptmann, Giselbert ; Steffensen, John Fleng ; Cao, Yihai. / Nitric oxide permits hypoxia-induced lymphatic perfusion by controlling arterial-lymphatic conduits in zebrafish and glass catfish. I: Proceedings of the National Academy of Science of the United States of America. 2009 ; Bind 106, Nr. 43. s. 18408-13.

Bibtex

@article{00a3bc00e65611deba73000ea68e967b,
title = "Nitric oxide permits hypoxia-induced lymphatic perfusion by controlling arterial-lymphatic conduits in zebrafish and glass catfish",
abstract = "The blood and lymphatic vasculatures are structurally and functionally coupled in controlling tissue perfusion, extracellular interstitial fluids, and immune surveillance. Little is known, however, about the molecular mechanisms that underlie the regulation of bloodlymphatic vessel connections and lymphatic perfusion. Here we show in the adult zebrafish and glass catfish (Kryptopterus bicirrhis) that blood-lymphatic conduits directly connect arterial vessels to the lymphatic system. Under hypoxic conditions, arterial-lymphatic conduits (ALCs) became highly dilated and linearized by NO-induced vascular relaxation, which led to blood perfusion into the lymphatic system. NO blockage almost completely abrogated hypoxia-induced ALC relaxation and lymphatic perfusion. These findings uncover mechanisms underlying hypoxia-induced oxygen compensation by perfusion of existing lymphatics in fish. Our results might also imply that the hypoxia-induced NO pathway contributes to development of progression of pathologies, including promotion of lymphatic metastasis by modulating arterial-lymphatic conduits, in the mammalian system.",
author = "{Dahl Ejby Jensen}, Lasse and Renhai Cao and Eva-Maria Hedlund and Iris S{\"o}ll and Lundberg, {Jon O} and Giselbert Hauptmann and Steffensen, {John Fleng} and Yihai Cao",
year = "2009",
doi = "10.1073/pnas.0907608106",
language = "English",
volume = "106",
pages = "18408--13",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
publisher = "The National Academy of Sciences of the United States of America",
number = "43",

}

RIS

TY - JOUR

T1 - Nitric oxide permits hypoxia-induced lymphatic perfusion by controlling arterial-lymphatic conduits in zebrafish and glass catfish

AU - Dahl Ejby Jensen, Lasse

AU - Cao, Renhai

AU - Hedlund, Eva-Maria

AU - Söll, Iris

AU - Lundberg, Jon O

AU - Hauptmann, Giselbert

AU - Steffensen, John Fleng

AU - Cao, Yihai

PY - 2009

Y1 - 2009

N2 - The blood and lymphatic vasculatures are structurally and functionally coupled in controlling tissue perfusion, extracellular interstitial fluids, and immune surveillance. Little is known, however, about the molecular mechanisms that underlie the regulation of bloodlymphatic vessel connections and lymphatic perfusion. Here we show in the adult zebrafish and glass catfish (Kryptopterus bicirrhis) that blood-lymphatic conduits directly connect arterial vessels to the lymphatic system. Under hypoxic conditions, arterial-lymphatic conduits (ALCs) became highly dilated and linearized by NO-induced vascular relaxation, which led to blood perfusion into the lymphatic system. NO blockage almost completely abrogated hypoxia-induced ALC relaxation and lymphatic perfusion. These findings uncover mechanisms underlying hypoxia-induced oxygen compensation by perfusion of existing lymphatics in fish. Our results might also imply that the hypoxia-induced NO pathway contributes to development of progression of pathologies, including promotion of lymphatic metastasis by modulating arterial-lymphatic conduits, in the mammalian system.

AB - The blood and lymphatic vasculatures are structurally and functionally coupled in controlling tissue perfusion, extracellular interstitial fluids, and immune surveillance. Little is known, however, about the molecular mechanisms that underlie the regulation of bloodlymphatic vessel connections and lymphatic perfusion. Here we show in the adult zebrafish and glass catfish (Kryptopterus bicirrhis) that blood-lymphatic conduits directly connect arterial vessels to the lymphatic system. Under hypoxic conditions, arterial-lymphatic conduits (ALCs) became highly dilated and linearized by NO-induced vascular relaxation, which led to blood perfusion into the lymphatic system. NO blockage almost completely abrogated hypoxia-induced ALC relaxation and lymphatic perfusion. These findings uncover mechanisms underlying hypoxia-induced oxygen compensation by perfusion of existing lymphatics in fish. Our results might also imply that the hypoxia-induced NO pathway contributes to development of progression of pathologies, including promotion of lymphatic metastasis by modulating arterial-lymphatic conduits, in the mammalian system.

U2 - 10.1073/pnas.0907608106

DO - 10.1073/pnas.0907608106

M3 - Journal article

C2 - 19822749

VL - 106

SP - 18408

EP - 18413

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 43

ER -

ID: 16239565