ArticleRespiratory research2010
Phosphodiesterase 6 subunits are expressed and altered in idiopathic pulmonary fibrosis.
Article in Respiratory research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Correction to: Phosphodiesterase 6 subunits are expressed and altered in idiopathic pulmonary fibrosis.Respiratory research · 2022Article
- Photoreceptor phosphodiesterase (PDE6): activation and inactivation mechanisms during visual transduction in rods and cones.Pflugers Archiv : European journal of physiology · 2021Review
- COVID19 Drug Repository: text-mining the literature in search of putative COVID19 therapeutics.Nucleic acids research · 2021Article
- Phosphodiesterase isoforms and cAMP compartments in the development of new therapies for obstructive pulmonary diseases.Current opinion in pharmacology · 2020Review
- Article
- Expression of phosphodiesterase 6 (PDE6) in human breast cancer cells.SpringerPlus · 2013Article
- The prenyl-binding protein PrBP/δ: a chaperone participating in intracellular trafficking.Vision research · 2012Review
- Cyclic nucleotide phosphodiesterase (PDE) isozymes as targets of the intracellular signalling network: benefits of PDE inhibitors in various diseases and perspectives for future therapeutic developments.British journal of pharmacology · 2012Review
- Arl2-GTP and Arl3-GTP regulate a GDI-like transport system for farnesylated cargo.Nature chemical biology · 2011Article
- Phosphodiesterase 6H, cone-specific inhibitor: Basis Sequence: Mouse.The AFCS-nature molecule pages · 2011Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIdiopathic Pulmonary Fibrosis (IPF) is an unresolved clinical issue. Phosphodiesterases (PDEs) are known therapeutic targets for various proliferative lung diseases. Lung PDE6 expression and function has received little or no attention. The present study aimed to characterize (i) PDE6 subunits expression in human lung, (ii) PDE6 subunits expression and alteration in IPF and (iii) functionality of the specific PDE6D subunit in alveolar epithelial cells (AECs). METHODOLOGY/PRINCIPAL
findingsPDE6 subunits expression in transplant donor (n = 6) and IPF (n = 6) lungs was demonstrated by real-time quantitative (q)RT-PCR and immunoblotting analysis. PDE6D mRNA and protein levels and PDE6G/H protein levels were significantly down-regulated in the IPF lungs. Immunohistochemical analysis showed alveolar epithelial localization of the PDE6 subunits. This was confirmed by qRT-PCR from human primary alveolar type (AT)II cells, demonstrating the down-regulation pattern of PDE6D in IPF-derived ATII cells. In vitro, PDE6D protein depletion was provoked by transforming growth factor (TGF)-β1 in A549 AECs. PDE6D siRNA-mediated knockdown and an ectopic expression of PDE6D modified the proliferation rate of A549 AECs. These effects were mediated by increased intracellular cGMP levels and decreased ERK phosphorylation. CONCLUSIONS/SIGNIFICANCE: Collectively, we report previously unrecognized PDE6 expression in human lungs, significant alterations of the PDE6D and PDE6G/H subunits in IPF lungs and characterize the functional role of PDE6D in AEC proliferation.
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