Peroxisome proliferator-activated receptor γ and ligands inhibit surfactant protein B gene expression in the lung

Li Yang, Dong Yan, Cong Yan, Hong Du

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Pulmonary nonciliated bronchiolar epithelial cells (Clara cells) and alveolar type II (AT II) epithelial cells are responsible for surfactant synthesis and secretion. These cells are highly lipogenic with a high lipid turnover rate. Although only 10% of surfactant lipids are neutral lipids, they play very important roles in maintaining pulmonary surfactant homeostasis. Many metabolic intermediate products of neutral lipids serve as ligands for various nuclear receptors that bind to target genes to influence gene transcription. In this report, the functional role of the neutral lipid metabolites, 15-deoxy-Δ12,14-prostaglandin J2 and 9-hydroxyoctadecanoic acids, and peroxisome proliferator-activated receptor γ was evaluated in surfactant protein B gene regulation. These reagents down-regulated surfactant protein B gene expression in respiratory epithelial cells at the transcriptional level in both cell line and whole lung explant systems. The studies support the concept that surfactant protein B homeostasis is influenced by neutral lipid metabolites in the lung.

Original languageEnglish (US)
Pages (from-to)36841-36847
Number of pages7
JournalJournal of Biological Chemistry
Volume278
Issue number38
DOIs
StatePublished - Sep 19 2003
Externally publishedYes

Fingerprint

Peroxisome Proliferator-Activated Receptors
Gene expression
Surface-Active Agents
Ligands
Lipids
Gene Expression
Lung
Metabolites
Homeostasis
Genes
Epithelial Cells
Alveolar Epithelial Cells
Pulmonary Surfactants
Transcription
Cytoplasmic and Nuclear Receptors
IgA receptor
Cells
Cell Line
Acids

ASJC Scopus subject areas

  • Biochemistry

Cite this

Peroxisome proliferator-activated receptor γ and ligands inhibit surfactant protein B gene expression in the lung. / Yang, Li; Yan, Dong; Yan, Cong; Du, Hong.

In: Journal of Biological Chemistry, Vol. 278, No. 38, 19.09.2003, p. 36841-36847.

Research output: Contribution to journalArticle

@article{8dcecb77f5124d0cb6f6bd4989365a54,
title = "Peroxisome proliferator-activated receptor γ and ligands inhibit surfactant protein B gene expression in the lung",
abstract = "Pulmonary nonciliated bronchiolar epithelial cells (Clara cells) and alveolar type II (AT II) epithelial cells are responsible for surfactant synthesis and secretion. These cells are highly lipogenic with a high lipid turnover rate. Although only 10{\%} of surfactant lipids are neutral lipids, they play very important roles in maintaining pulmonary surfactant homeostasis. Many metabolic intermediate products of neutral lipids serve as ligands for various nuclear receptors that bind to target genes to influence gene transcription. In this report, the functional role of the neutral lipid metabolites, 15-deoxy-Δ12,14-prostaglandin J2 and 9-hydroxyoctadecanoic acids, and peroxisome proliferator-activated receptor γ was evaluated in surfactant protein B gene regulation. These reagents down-regulated surfactant protein B gene expression in respiratory epithelial cells at the transcriptional level in both cell line and whole lung explant systems. The studies support the concept that surfactant protein B homeostasis is influenced by neutral lipid metabolites in the lung.",
author = "Li Yang and Dong Yan and Cong Yan and Hong Du",
year = "2003",
month = "9",
day = "19",
doi = "10.1074/jbc.M304156200",
language = "English (US)",
volume = "278",
pages = "36841--36847",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "38",

}

TY - JOUR

T1 - Peroxisome proliferator-activated receptor γ and ligands inhibit surfactant protein B gene expression in the lung

AU - Yang, Li

AU - Yan, Dong

AU - Yan, Cong

AU - Du, Hong

PY - 2003/9/19

Y1 - 2003/9/19

N2 - Pulmonary nonciliated bronchiolar epithelial cells (Clara cells) and alveolar type II (AT II) epithelial cells are responsible for surfactant synthesis and secretion. These cells are highly lipogenic with a high lipid turnover rate. Although only 10% of surfactant lipids are neutral lipids, they play very important roles in maintaining pulmonary surfactant homeostasis. Many metabolic intermediate products of neutral lipids serve as ligands for various nuclear receptors that bind to target genes to influence gene transcription. In this report, the functional role of the neutral lipid metabolites, 15-deoxy-Δ12,14-prostaglandin J2 and 9-hydroxyoctadecanoic acids, and peroxisome proliferator-activated receptor γ was evaluated in surfactant protein B gene regulation. These reagents down-regulated surfactant protein B gene expression in respiratory epithelial cells at the transcriptional level in both cell line and whole lung explant systems. The studies support the concept that surfactant protein B homeostasis is influenced by neutral lipid metabolites in the lung.

AB - Pulmonary nonciliated bronchiolar epithelial cells (Clara cells) and alveolar type II (AT II) epithelial cells are responsible for surfactant synthesis and secretion. These cells are highly lipogenic with a high lipid turnover rate. Although only 10% of surfactant lipids are neutral lipids, they play very important roles in maintaining pulmonary surfactant homeostasis. Many metabolic intermediate products of neutral lipids serve as ligands for various nuclear receptors that bind to target genes to influence gene transcription. In this report, the functional role of the neutral lipid metabolites, 15-deoxy-Δ12,14-prostaglandin J2 and 9-hydroxyoctadecanoic acids, and peroxisome proliferator-activated receptor γ was evaluated in surfactant protein B gene regulation. These reagents down-regulated surfactant protein B gene expression in respiratory epithelial cells at the transcriptional level in both cell line and whole lung explant systems. The studies support the concept that surfactant protein B homeostasis is influenced by neutral lipid metabolites in the lung.

UR - http://www.scopus.com/inward/record.url?scp=0141480282&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0141480282&partnerID=8YFLogxK

U2 - 10.1074/jbc.M304156200

DO - 10.1074/jbc.M304156200

M3 - Article

VL - 278

SP - 36841

EP - 36847

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 38

ER -