Impact of litter size on survival, growth and lung alveolarization of newborn mouse pups.


Journal

Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft
ISSN: 1618-0402
Titre abrégé: Ann Anat
Pays: Germany
ID NLM: 100963897

Informations de publication

Date de publication:
Nov 2020
Historique:
received: 03 05 2020
revised: 24 06 2020
accepted: 25 06 2020
pubmed: 21 7 2020
medline: 28 7 2021
entrez: 21 7 2020
Statut: ppublish

Résumé

Lung alveolarization, the development of the alveoli, is disturbed in preterm infants with bronchopulmonary dysplasia (BPD), the most common complication of preterm birth. Animal models based on oxygen toxicity to the developing mouse lung are used to understand the mechanisms of stunted alveolarization in BPD, and to develop new medical management strategies for affected infants. The toxicity of genetic and pharmacological interventions, together with maternal cannibalism, reduce mouse litter sizes in experimental studies. The impact of litter size on normal and stunted lung alveolarization is unknown, but may influence data interpretation. The aim of the study was to assess the impact of litter size on normal and oxygen-stunted lung alveolarization in mice. BPD was experimentally modelled in newborn C57BL/6J mice by exposure to 85% O Litter sizes of a single mouse were not viable to post-natal day 14. Normal lung alveolarization was comparable in mouse pups in litters of 2, 4, 6, and 8 pups per litter. Hyperoxia was equally effective at stunting lung alveolarization in mouse pups in litters of 2, 4, 6, and 8 pups per litter. Studies on normal lung alveolarization as well as alveolarization stunted by oxygen toxicity can be undertaken in mouse litters as small as two pups, and as large as eight pups. There is no evidence to suggest that data cannot be compared within and between litters of two to eight mouse pups.

Sections du résumé

BACKGROUND BACKGROUND
Lung alveolarization, the development of the alveoli, is disturbed in preterm infants with bronchopulmonary dysplasia (BPD), the most common complication of preterm birth. Animal models based on oxygen toxicity to the developing mouse lung are used to understand the mechanisms of stunted alveolarization in BPD, and to develop new medical management strategies for affected infants. The toxicity of genetic and pharmacological interventions, together with maternal cannibalism, reduce mouse litter sizes in experimental studies. The impact of litter size on normal and stunted lung alveolarization is unknown, but may influence data interpretation. The aim of the study was to assess the impact of litter size on normal and oxygen-stunted lung alveolarization in mice.
METHODS METHODS
BPD was experimentally modelled in newborn C57BL/6J mice by exposure to 85% O
RESULTS RESULTS
Litter sizes of a single mouse were not viable to post-natal day 14. Normal lung alveolarization was comparable in mouse pups in litters of 2, 4, 6, and 8 pups per litter. Hyperoxia was equally effective at stunting lung alveolarization in mouse pups in litters of 2, 4, 6, and 8 pups per litter.
CONCLUSIONS CONCLUSIONS
Studies on normal lung alveolarization as well as alveolarization stunted by oxygen toxicity can be undertaken in mouse litters as small as two pups, and as large as eight pups. There is no evidence to suggest that data cannot be compared within and between litters of two to eight mouse pups.

Identifiants

pubmed: 32688019
pii: S0940-9602(20)30123-0
doi: 10.1016/j.aanat.2020.151579
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

151579

Informations de copyright

Copyright © 2020 Elsevier GmbH. All rights reserved.

Auteurs

Sophie Feddersen (S)

Department of Lung Development and Remodelling, Max Planck Institute for Heart and Lung Research, Parkstrasse 1, 60231 Bad Nauheim, Germany; Department of Internal Medicine (Pulmonology), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University, Aulweg 123, 35392 Giessen, Germany.

Claudio Nardiello (C)

Department of Lung Development and Remodelling, Max Planck Institute for Heart and Lung Research, Parkstrasse 1, 60231 Bad Nauheim, Germany; Department of Internal Medicine (Pulmonology), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University, Aulweg 123, 35392 Giessen, Germany.

Balachandar Selvakumar (B)

Department of Internal Medicine (Pulmonology), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University, Aulweg 123, 35392 Giessen, Germany; Instituto de Investigación en Biomedicina de Buenos Aires, Godoy Cruz 2390, C1425FQD Ciudad Autónoma de Buenos Aires, Argentina.

István Vadász (I)

Department of Internal Medicine (Pulmonology), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University, Aulweg 123, 35392 Giessen, Germany.

Susanne Herold (S)

Department of Internal Medicine (Pulmonology), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University, Aulweg 123, 35392 Giessen, Germany.

Werner Seeger (W)

Department of Lung Development and Remodelling, Max Planck Institute for Heart and Lung Research, Parkstrasse 1, 60231 Bad Nauheim, Germany; Department of Internal Medicine (Pulmonology), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University, Aulweg 123, 35392 Giessen, Germany.

Rory E Morty (RE)

Department of Lung Development and Remodelling, Max Planck Institute for Heart and Lung Research, Parkstrasse 1, 60231 Bad Nauheim, Germany; Department of Internal Medicine (Pulmonology), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University, Aulweg 123, 35392 Giessen, Germany. Electronic address: rory.morty@mpi-bn.mpg.de.

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Classifications MeSH