Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Lung inflammatory injury and tissue repair (Jul 2023)
    • Immune Environment in Glioblastoma (Feb 2023)
    • Korsmeyer Award 25th Anniversary Collection (Jan 2023)
    • Aging (Jul 2022)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Research letters
    • Letters to the editor
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Research letters
  • Letters to the editor
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Version history
  • Article usage
  • Citations to this article

Advertisement

CorrigendumPulmonology Free access | 10.1172/JCI38061C1

LPCAT1 regulates surfactant phospholipid synthesis and is required for transitioning to air breathing in mice

James P. Bridges, Machiko Ikegami, Lauren L. Brilli, Xueni Chen, Robert J. Mason, and John M. Shannon

Find articles by Bridges, J. in: JCI | PubMed | Google Scholar

Find articles by Ikegami, M. in: JCI | PubMed | Google Scholar

Find articles by Brilli, L. in: JCI | PubMed | Google Scholar

Find articles by Chen, X. in: JCI | PubMed | Google Scholar

Find articles by Mason, R. in: JCI | PubMed | Google Scholar

Find articles by Shannon, J. in: JCI | PubMed | Google Scholar

Published June 1, 2010 - More info

Published in Volume 120, Issue 6 on June 1, 2010
J Clin Invest. 2010;120(6):2248–2248. https://doi.org/10.1172/JCI38061C1.
© 2010 The American Society for Clinical Investigation
Published June 1, 2010 - Version history
View PDF

Related article:

LPCAT1 regulates surfactant phospholipid synthesis and is required for transitioning to air breathing in mice
James P. Bridges, … , Robert J. Mason, John M. Shannon
James P. Bridges, … , Robert J. Mason, John M. Shannon
Research Article Pulmonology

LPCAT1 regulates surfactant phospholipid synthesis and is required for transitioning to air breathing in mice

  • Text
  • PDF
Abstract

Respiratory distress syndrome (RDS), which is the leading cause of death in premature infants, is caused by surfactant deficiency. The most critical and abundant phospholipid in pulmonary surfactant is saturated phosphatidylcholine (SatPC), which is synthesized in alveolar type II cells de novo or by the deacylation-reacylation of existing phosphatidylcholine species. We recently cloned and partially characterized a mouse enzyme with characteristics of a lung lysophosphatidylcholine acyltransferase (LPCAT1) that we predicted would be involved in surfactant synthesis. Here, we describe our studies investigating whether LPCAT1 is required for pulmonary surfactant homeostasis. To address this issue, we generated mice bearing a hypomorphic allele of Lpcat1 (referred to herein as Lpcat1GT/GT mice) using a genetrap strategy. Newborn Lpcat1GT/GT mice showed varying perinatal mortality from respiratory failure, with affected animals demonstrating hallmarks of respiratory distress such as atelectasis and hyaline membranes. Lpcat1 mRNA levels were reduced in newborn Lpcat1GT/GT mice and directly correlated with SatPC content, LPCAT1 activity, and survival. Surfactant isolated from dead Lpcat1GT/GT mice failed to reduce minimum surface tension to wild-type levels. Collectively, these data demonstrate that full LPCAT1 activity is required to achieve the levels of SatPC essential for the transition to air breathing.

Authors

James P. Bridges, Machiko Ikegami, Lauren L. Brilli, Xueni Chen, Robert J. Mason, John M. Shannon

×

Original citation: J Clin Invest.2010;120(5):1736–1748. doi:10.1172/JCI38061.

Citation for this corrigendum: J Clin Invest. 2010;120(6):2248. doi:10.1172/JCI38061C1.

In Figure 5C, the fourth immunoblot from the top was inadvertently mislabeled. The correct Figure 5C appears below.

Figure 5

The authors regret the error.

Version history
  • Version 1 (June 1, 2010): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Version history
Advertisement
Advertisement

Copyright © 2023 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts