Regulation of Clara cell secretory protein gene expression by the CCAAT-binding factor NF-Y

2007 ◽  
Vol 459 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Adriana Acosta ◽  
Teresa Zariñán ◽  
Héctor Macías ◽  
Ana María Pasapera ◽  
Marco Allán Pérez-Solis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Gene ◽  
Secretory Protein ◽  
Clara Cell ◽  
Clara Cell Secretory Protein ◽  
Binding Factor

Structure and Regulation of the Murine Clara Cell Secretory Protein Gene

Genomics ◽  
1994 ◽  
Vol 20 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Barry R. Stripp ◽  
Jacquelyn A. Huffman ◽  
Robert J. Bohinski
Keyword(s):  
Protein Gene ◽  
Secretory Protein ◽  
Clara Cell ◽  
Clara Cell Secretory Protein

C/EBP α and C/EBP δ Activate the Clara Cell Secretory Protein Gene through Interaction with Two Adjacent C/EBP-Binding Sites

2000 ◽  
Vol 22 (4) ◽  
pp. 469-480 ◽  
Author(s):  
Tobias N. Cassel ◽  
Lena Nordlund-Möller ◽  
Olof Andersson ◽  
Jan-Åke Gustafsson ◽  
Magnus Nord
Keyword(s):  
Binding Sites ◽  
Protein Gene ◽  
Secretory Protein ◽  
Clara Cell ◽  
Clara Cell Secretory Protein

cDNA sequence, 5′-flanking region, and promoter activity of the Neotomodon alstoni alstoni Clara cell secretory protein gene

2004 ◽  
Vol 427 (2) ◽  
pp. 170-179 ◽  
Author(s):  
Héctor Macı́as ◽  
Ana Marı́a Pasapera ◽  
Marco Allán Pérez-Solis ◽  
Alfredo Ulloa-Aguirre ◽  
Rubén Gutiérrez-Sagal
Keyword(s):  
Promoter Activity ◽  
Cdna Sequence ◽  
Protein Gene ◽  
Secretory Protein ◽  
Clara Cell ◽  
Clara Cell Secretory Protein ◽  
Flanking Region

Interferon-γ stimulates human Clara cell secretory protein production by human airway epithelial cells

1998 ◽  
Vol 274 (5) ◽  
pp. L864-L869 ◽  
Author(s):  
X. L. Yao ◽  
T. Ikezono ◽  
M. Cowan ◽  
C. Logun ◽  
C. W. Angus ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Synthesis ◽  
Epithelial Cells ◽  
Secretory Protein ◽  
Airway Epithelial Cells ◽  
Clara Cell ◽  
Dependent Manner ◽  
Airway Epithelial ◽  
Clara Cell Secretory Protein ◽  
Ifn Γ

Clara cell secretory protein (CCSP) is an inhibitor of secretory phospholipase A2. It is produced by airway epithelial cells and is present in airway secretions. Because interferon (IFN)-γ can induce gene expression in airway epithelial cells and may modulate the inflammatory response in the airway, it was of interest to study the effect of this cytokine on epithelial cell CCSP mRNA expression and CCSP protein synthesis. A human bronchial epithelial cell line (BEAS-2B) was used for this study. CCSP mRNA was detected by ribonuclease protection assay. IFN-γ was found to increase CCSP mRNA expression in a time- and dose-dependent manner. The CCSP mRNA level increased after IFN-γ (300 U/ml) treatment for 8–36 h, with the peak increase at 18 h. Immunobloting of CCSP protein also demonstrated that IFN-γ induced the synthesis and secretion of CCSP protein in a time-dependent manner. Nuclear run-on, CCSP reporter gene activity assay, and CCSP mRNA half-life assay demonstrated that IFN-γ-induced increases in CCSP gene expression were mediated, at least in part, at the posttranscriptional level. The present study demonstrates that IFN-γ can induce increases in steady-state mRNA levels and protein synthesis of human CCSP protein in airway epithelial cells and may modulate airway inflammatory responses in this manner.

Multiple mechanisms for oxygen‐induced regulation of the Clara cell secretory protein gene

2003 ◽  
Vol 17 (14) ◽  
pp. 1-22 ◽  
Author(s):  
Patricia L. Ramsay ◽  
Ziqiang Luo ◽  
Angela Major ◽  
Moon S. Park ◽  
Milton Finegold ◽  
...  
Keyword(s):  
Protein Gene ◽  
Secretory Protein ◽  
Clara Cell ◽  
Clara Cell Secretory Protein

scholarly journals Clara Cell Secretory Protein Is Reduced in Equine Recurrent Airway Obstruction

2009 ◽  
Vol 46 (4) ◽  
pp. 604-613 ◽  
Author(s):  
P. Katavolos ◽  
C. A. Ackerley ◽  
L. Viel ◽  
M. E. Clark ◽  
X. Wen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Airway Obstruction ◽  
Secretory Protein ◽  
Lung Lavage ◽  
Clara Cell ◽  
Immunogold Label ◽  
Recurrent Airway Obstruction ◽  
Clara Cell Secretory Protein ◽  
Before And After ◽  
Active Disease

Horses are prone to recurrent airway obstruction (RAO), an inflammatory lung disease induced by repeated exposure to environmental mold, dust, and bacterial components. Active disease manifests with mucus hyperproduction, neutrophilic inflammation, bronchoconstriction, and coughing. Chronically affected animals have lung remodeling characterized by smooth muscle hyperplasia, collagen deposition, lymphoid hyperplasia, and impaired aerobic performance. Clara cell secretory protein (CCSP) counters inflammation in the lung, hence we hypothesized that CCSP depletion is a key feature of RAO in horses. Recombinant equine CCSP and specific antiserum were produced, and percutaneous lung biopsies were obtained from 3 healthy horses and from 3 RAO-affected horses before and after induction of RAO. CCSP relative gene expression in tissue, as well as protein concentration in lung lavage fluid, was determined. Immunocytochemical analysis, using both light and immunogold ultrastructural methods, demonstrated reduced CCSP staining in lung tissue of animals with RAO. Immunogold label in Clara cell granules was less in animals with chronic RAO than in normal animals, and absent in animals that had active disease. Median lung lavage CCSP concentration was 132 and 129 ng/ml in healthy horses, and 62 and 24 ng/ml in RAO horses before and after challenge, respectively. CCSP lung gene expression was significantly higher in healthy animals than in animals with chronic RAO. Together, these preliminary findings suggest that reduced production of CCSP and subcellular changes in Clara cells are features of chronic environmentally induced lung inflammation in horses.

Clara cell secretory protein gene expression in bronchiolar epithelium

1992 ◽  
Vol 262 (4) ◽  
pp. L399-L404 ◽  
Author(s):  
B. P. Hackett ◽  
N. Shimizu ◽  
J. D. Gitlin
Keyword(s):  
Gene Expression ◽  
Lung Tissue ◽  
Prolonged Exposure ◽  
Secretory Protein ◽  
Clara Cell ◽  
Fetal Life ◽  
Clara Cells ◽  
Adult Rats ◽  
Clara Cell Secretory Protein ◽  
Bronchiolar Epithelium

To determine the mechanisms of Clara cell secretory protein (CCSP) gene expression, a cDNA clone was isolated and used in RNA blot analysis. A single 600 bp CCSP specific transcript was detected in the developing rat lung on fetal day 18. This transcript increased in abundance during late fetal life such that adult levels were attained within 2 wk postpartum. CCSP gene expression was tissue specific, being confined to lung and trachea at all developmental stages. The abundance of CCSP mRNA in lung tissue was unchanged after the induction of lung injury in adult rats either with lipopolysaccharide or prolonged exposure to hyperoxia. In situ hybridization of lung tissue revealed that CCSP gene expression is localized to the nonciliated epithelial (Clara) cells of the bronchiolar epithelium throughout fetal and postnatal development. Taken together the results indicate that the gene for CCSP is abundantly expressed in a cell-specific fashion in the lung and suggest that analysis of such expression will be useful in elucidating the role of Clara cells in the growth and development of the bronchiolar epithelium.

scholarly journals Role of hepatocyte nuclear factor-3α and hepatocyte nuclear factor-3β in Clara cell secretory protein gene expression in the bronchiolar epithelium

1995 ◽  
Vol 308 (1) ◽  
pp. 197-202 ◽  
Author(s):  
C D Bingle ◽  
B P Hackett ◽  
M Moxley ◽  
W Longmore ◽  
J D Gitlin
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Secretory Protein ◽  
Clara Cell ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Clara Cell Secretory Protein ◽  
Region I ◽  
Bronchiolar Epithelium

The 5′ flanking region of the Clara cell secretory protein (CCSP) gene contains two cis-acting elements which bind hepatocyte nuclear factor (HNF)-3 alpha and HNF-3 beta in vitro. To determine the role of these proteins in mediating CCSP gene expression in the bronchiolar epithelium, chimeric CCSP-reporter gene constructs containing various regions of the CCSP 5′ flanking region were co-transfected into H-441 cells with HNF-3 alpha or HNF-3 beta expression plasmids. These studies indicate that each of these transcription factors positively regulates CCSP gene expression and revealed that CCSP region I (-132 to -76) is sufficient to mediate this effect. Gel-mobility-shift assays with oligonucleotides corresponding to CCSP region I, nuclear extract from bronchiolar epithelial cells and HNF-3-specific antibodies indicate that HNF-3 alpha and HNF-3 beta are the only proteins in bronchiolar epithelial cells which directly interact with this region. Consistent with these observations, HNF-3 alpha and HNF-3 beta transcripts were found to be enriched in this cell population and in situ hybridization of adult lung revealed HNF-3 gene expression in non-ciliated bronchiolar epithelial cells expressing the CCSP gene. Finally, experiments with CCSP region I and a heterologous promoter indicate that this region acts in a promoter-specific context, suggesting that additional factors interacting via the minimal CCSP promoter region are essential in determining the effects of HNF-3 on cell-specific CCSP gene expression in the bronchiolar epithelium.

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