Glucagon-Like Peptide 1 and Atrial Natriuretic Peptide in a Female Mouse Model of Obstructive Pulmonary Disease

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Standard

Glucagon-Like Peptide 1 and Atrial Natriuretic Peptide in a Female Mouse Model of Obstructive Pulmonary Disease. / Balk-Møller, Emilie; Windeløv, Johanne Agerlin; Svendsen, Berit; Hunt, Jenna; Ghiasi, Seyed Mojtaba; Sørensen, Charlotte Mehlin; Holst, Jens Juul; Kissow, Hannelouise.

I: Endocrine Research, Bind 4, Nr. 1, bvz034, 2020.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Balk-Møller, E, Windeløv, JA, Svendsen, B, Hunt, J, Ghiasi, SM, Sørensen, CM, Holst, JJ & Kissow, H 2020, 'Glucagon-Like Peptide 1 and Atrial Natriuretic Peptide in a Female Mouse Model of Obstructive Pulmonary Disease', Endocrine Research, bind 4, nr. 1, bvz034. https://doi.org/10.1210/jendso/bvz034

APA

Balk-Møller, E., Windeløv, J. A., Svendsen, B., Hunt, J., Ghiasi, S. M., Sørensen, C. M., ... Kissow, H. (2020). Glucagon-Like Peptide 1 and Atrial Natriuretic Peptide in a Female Mouse Model of Obstructive Pulmonary Disease. Endocrine Research, 4(1), [bvz034]. https://doi.org/10.1210/jendso/bvz034

Vancouver

Balk-Møller E, Windeløv JA, Svendsen B, Hunt J, Ghiasi SM, Sørensen CM o.a. Glucagon-Like Peptide 1 and Atrial Natriuretic Peptide in a Female Mouse Model of Obstructive Pulmonary Disease. Endocrine Research. 2020;4(1). bvz034. https://doi.org/10.1210/jendso/bvz034

Author

Balk-Møller, Emilie ; Windeløv, Johanne Agerlin ; Svendsen, Berit ; Hunt, Jenna ; Ghiasi, Seyed Mojtaba ; Sørensen, Charlotte Mehlin ; Holst, Jens Juul ; Kissow, Hannelouise. / Glucagon-Like Peptide 1 and Atrial Natriuretic Peptide in a Female Mouse Model of Obstructive Pulmonary Disease. I: Endocrine Research. 2020 ; Bind 4, Nr. 1.

Bibtex

@article{65961b2f1981425f967b15f5ccee0db2,
title = "Glucagon-Like Peptide 1 and Atrial Natriuretic Peptide in a Female Mouse Model of Obstructive Pulmonary Disease",
abstract = "Glucagon-like peptide-1 (GLP-1) is protective in lung disease models but the underlying mechanisms remain elusive. Because the hormone atrial natriuretic peptide (ANP) also has beneficial effects in lung disease, we hypothesized that GLP-1 effects may be mediated by ANP expression. To study this putative link, we used a mouse model of chronic obstructive pulmonary disease (COPD) and assessed lung function by unrestrained whole-body plethysmography. In 1 study, we investigated the role of endogenous GLP-1 by genetic GLP-1 receptor (GLP-1R) knockout (KO) and pharmaceutical blockade of the GLP-1R with the antagonist exendin-9 to -39 (EX-9). In another study the effects of exogenous GLP-1 were assessed. Lastly, we investigated the bronchodilatory properties of ANP and a GLP-1R agonist on isolated bronchial sections from healthy and COPD mice. Lung function did not differ between mice receiving phosphate-buffered saline (PBS) and EX-9 or between GLP-1R KO mice and their wild-type littermates. The COPD mice receiving GLP-1R agonist improved pulmonary function (P < .01) with less inflammation, but no less emphysema compared to PBS-treated mice. Compared with the PBS-treated mice, treatment with GLP-1 agonist increased ANP (nppa) gene expression by 10-fold (P < .01) and decreased endothelin-1 (P < .01), a peptide associated with bronchoconstriction. ANP had moderate bronchodilatory effects in isolated bronchial sections and GLP-1R agonist also showed bronchodilatory properties but less than ANP. Responses to both peptides were significantly increased in COPD mice (P < .05, P < .01). Taken together, our study suggests a link between GLP-1 and ANP in COPD.",
author = "Emilie Balk-M{\o}ller and Windel{\o}v, {Johanne Agerlin} and Berit Svendsen and Jenna Hunt and Ghiasi, {Seyed Mojtaba} and S{\o}rensen, {Charlotte Mehlin} and Holst, {Jens Juul} and Hannelouise Kissow",
note = "{\circledC} Endocrine Society 2019.",
year = "2020",
doi = "10.1210/jendso/bvz034",
language = "English",
volume = "4",
journal = "Endocrine Research",
issn = "0743-5800",
publisher = "Taylor & Francis",
number = "1",

}

RIS

TY - JOUR

T1 - Glucagon-Like Peptide 1 and Atrial Natriuretic Peptide in a Female Mouse Model of Obstructive Pulmonary Disease

AU - Balk-Møller, Emilie

AU - Windeløv, Johanne Agerlin

AU - Svendsen, Berit

AU - Hunt, Jenna

AU - Ghiasi, Seyed Mojtaba

AU - Sørensen, Charlotte Mehlin

AU - Holst, Jens Juul

AU - Kissow, Hannelouise

N1 - © Endocrine Society 2019.

PY - 2020

Y1 - 2020

N2 - Glucagon-like peptide-1 (GLP-1) is protective in lung disease models but the underlying mechanisms remain elusive. Because the hormone atrial natriuretic peptide (ANP) also has beneficial effects in lung disease, we hypothesized that GLP-1 effects may be mediated by ANP expression. To study this putative link, we used a mouse model of chronic obstructive pulmonary disease (COPD) and assessed lung function by unrestrained whole-body plethysmography. In 1 study, we investigated the role of endogenous GLP-1 by genetic GLP-1 receptor (GLP-1R) knockout (KO) and pharmaceutical blockade of the GLP-1R with the antagonist exendin-9 to -39 (EX-9). In another study the effects of exogenous GLP-1 were assessed. Lastly, we investigated the bronchodilatory properties of ANP and a GLP-1R agonist on isolated bronchial sections from healthy and COPD mice. Lung function did not differ between mice receiving phosphate-buffered saline (PBS) and EX-9 or between GLP-1R KO mice and their wild-type littermates. The COPD mice receiving GLP-1R agonist improved pulmonary function (P < .01) with less inflammation, but no less emphysema compared to PBS-treated mice. Compared with the PBS-treated mice, treatment with GLP-1 agonist increased ANP (nppa) gene expression by 10-fold (P < .01) and decreased endothelin-1 (P < .01), a peptide associated with bronchoconstriction. ANP had moderate bronchodilatory effects in isolated bronchial sections and GLP-1R agonist also showed bronchodilatory properties but less than ANP. Responses to both peptides were significantly increased in COPD mice (P < .05, P < .01). Taken together, our study suggests a link between GLP-1 and ANP in COPD.

AB - Glucagon-like peptide-1 (GLP-1) is protective in lung disease models but the underlying mechanisms remain elusive. Because the hormone atrial natriuretic peptide (ANP) also has beneficial effects in lung disease, we hypothesized that GLP-1 effects may be mediated by ANP expression. To study this putative link, we used a mouse model of chronic obstructive pulmonary disease (COPD) and assessed lung function by unrestrained whole-body plethysmography. In 1 study, we investigated the role of endogenous GLP-1 by genetic GLP-1 receptor (GLP-1R) knockout (KO) and pharmaceutical blockade of the GLP-1R with the antagonist exendin-9 to -39 (EX-9). In another study the effects of exogenous GLP-1 were assessed. Lastly, we investigated the bronchodilatory properties of ANP and a GLP-1R agonist on isolated bronchial sections from healthy and COPD mice. Lung function did not differ between mice receiving phosphate-buffered saline (PBS) and EX-9 or between GLP-1R KO mice and their wild-type littermates. The COPD mice receiving GLP-1R agonist improved pulmonary function (P < .01) with less inflammation, but no less emphysema compared to PBS-treated mice. Compared with the PBS-treated mice, treatment with GLP-1 agonist increased ANP (nppa) gene expression by 10-fold (P < .01) and decreased endothelin-1 (P < .01), a peptide associated with bronchoconstriction. ANP had moderate bronchodilatory effects in isolated bronchial sections and GLP-1R agonist also showed bronchodilatory properties but less than ANP. Responses to both peptides were significantly increased in COPD mice (P < .05, P < .01). Taken together, our study suggests a link between GLP-1 and ANP in COPD.

U2 - 10.1210/jendso/bvz034

DO - 10.1210/jendso/bvz034

M3 - Journal article

C2 - 32010874

VL - 4

JO - Endocrine Research

JF - Endocrine Research

SN - 0743-5800

IS - 1

M1 - bvz034

ER -

ID: 235923115