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Loss of phosphatase and tensin homolog (PTEN) induces leptin-mediated leptin gene expression: feed-forward loop operating in the lung.
- Source :
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The Journal of biological chemistry [J Biol Chem] 2013 Oct 11; Vol. 288 (41), pp. 29821-35. Date of Electronic Publication: 2013 Aug 20. - Publication Year :
- 2013
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Abstract
- Elevated levels of systemic and pulmonary leptin are associated with diseases related to lung injury and lung cancer. However, the role of leptin in lung biology and pathology, including the mechanism of leptin gene expression in the pathogenesis of lung diseases, including lung cancer, remains elusive. Here, using conditional deletion of tumor suppressor gene Pten in the lung epithelium in vivo in transgenic mice and human PTEN-null lung epithelial cells, we identify the leptin-driven feed-forward signaling loop in the lung epithelial cells. Leptin-mediated leptin/leptin-receptor gene expression likely amplifies leptin signaling that may contribute to the pathogenesis and severity of lung diseases, resulting in poor clinical outcomes. Loss of Pten in the lung epithelial cells in vivo activated adipokine signaling and induced leptin synthesis as ascertained by genome-wide mRNA profiling and pathway analysis. Leptin gene transcription was mediated by binding of transcription factors NRF-1 and CCAAT/enhancer-binding protein δ (C/EBP) to the proximal promoter regions and STAT3 to the distal promoter regions as revealed by leptin promoter-mutation, chromatin immunoprecipitation, and gain- and loss-of-function studies in lung epithelial cells. Leptin treatment induced expression of the leptin/leptin receptor in the lung epithelial cells via activation of MEK/ERK, PI3K/AKT/mammalian target of rapamycin (mTOR), and JAK2/STAT3 signaling pathways. Expression of constitutively active MEK-1, AKT, and STAT3 proteins increased expression, and treatment with MEK, PI3K, AKT, and mTOR inhibitors decreased LEP expression, indicating that leptin via MAPK/ERK1/2, PI3K/AKT/mTOR, and JAK2/STAT3 pathways, in turn, further induces its own gene expression. Thus, targeted inhibition of the leptin-mediated feed-forward loop provides a novel rationale for pharmacotherapy of disease associated with lung injury and remodeling, including lung cancer.
- Subjects :
- Adipocytes drug effects
Adipocytes metabolism
Animals
CCAAT-Enhancer-Binding Protein-delta genetics
CCAAT-Enhancer-Binding Protein-delta metabolism
Cell Line, Tumor
Gene Expression drug effects
Gene Expression Profiling
Humans
Immunohistochemistry
Leptin metabolism
Leptin pharmacology
Lung pathology
Mice
Mice, Knockout
Mice, Transgenic
Mitogen-Activated Protein Kinase Kinases genetics
Mitogen-Activated Protein Kinase Kinases metabolism
NF-E2-Related Factor 1 genetics
NF-E2-Related Factor 1 metabolism
Oligonucleotide Array Sequence Analysis
PTEN Phosphohydrolase metabolism
Phosphatidylinositol 3-Kinases genetics
Phosphatidylinositol 3-Kinases metabolism
Promoter Regions, Genetic genetics
Protein Binding
RNA Interference
Receptors, Leptin metabolism
Reverse Transcriptase Polymerase Chain Reaction
STAT3 Transcription Factor genetics
STAT3 Transcription Factor metabolism
Signal Transduction drug effects
Signal Transduction genetics
Leptin genetics
Lung metabolism
PTEN Phosphohydrolase genetics
Receptors, Leptin genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1083-351X
- Volume :
- 288
- Issue :
- 41
- Database :
- MEDLINE
- Journal :
- The Journal of biological chemistry
- Publication Type :
- Academic Journal
- Accession number :
- 23963458
- Full Text :
- https://doi.org/10.1074/jbc.M113.481523