Interferon-gamma regulation of Clara cell gene expression: in vivo and in vitro
| Autor: | R. H. Costa, M. K. Ray, Stephen E. Welty, G. Wang, Kathy J. Jackson, Francesco J. DeMayo, Susan Magdaleno |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Hepatocyte Nuclear Factor 3-alpha
Male Pulmonary and Respiratory Medicine medicine.medical_specialty Transcription Genetic Physiology Mice Transgenic Polymerase Chain Reaction Interferon-gamma Mice Transcription (biology) Physiology (medical) Internal medicine Gene expression medicine Animals Uteroglobin Interferon gamma RNA Messenger STAT1 Enzyme Inhibitors Binding site Promoter Regions Genetic Lung Cell Line Transformed DNA Primers Cell Nucleus Mice Inbred ICR Messenger RNA biology Nuclear Proteins Proteins Cell Biology respiratory system Molecular biology Recombinant Proteins DNA-Binding Proteins Hepatocyte nuclear factors Endocrinology Protein Biosynthesis Hepatocyte Nuclear Factor 3-beta biology.protein STAT protein Female Transcription Factors medicine.drug |
| Zdroj: | ResearcherID |
| ISSN: | 1522-1504 1040-0605 |
| DOI: | 10.1152/ajplung.1997.272.6.l1142 |
| Popis: | This report demonstrates that Clara cell 10-kDa protein (CC10) mRNA levels are regulated by interferon-gamma (IFN-gamma). An analysis of total lung RNA from mice given IFN-gamma intratracheally showed increased levels of CC10 mRNA compared to control animals but no significant increases in surfactant proteins B and C. These results were confirmed in a Clara cell line, mtCC1-2, generated from the lungs of a transgenic mouse expressing the SV40 large T antigen under the control of a Clara cell-specific promoter. Significant increases in mtCC1-2 CC10 mRNA levels were observed in a time- and a dose-dependent manner. The expression of transacting factors hepatocyte nuclear factors 3 alpha and 3 beta (HNF-3 alpha and HNF-3 beta) were also analyzed, and a transient increase in the expression of HNF-3 beta but not HNF-3 alpha was detected. Deoxyribonuclease I footprint analysis identified a signal transducer and activator of transcription (STAT) binding site (at nucleotides -293 to -284 of CC10) adjacent to two thyroid transcription factor-1 (TTF-1) binding sites, suggesting a potential interaction between STAT1 and TTF-1. This report reinforces the hypothesis that CC10 functions as an anti-inflammatory protein and that increases in CC10 protein may provide additional protection from inflammation and disease in the lung. |
| Databáze: | OpenAIRE |
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