The Expression of Clara Cell Secretory Protein in BAL Fluid of Patients with Idiopathic Interstitial Pneumonia

2002 ◽  
Vol 53 (2) ◽  
pp. 127
Author(s):  
Sang Won Um ◽  
Seon Jin Han ◽  
Chang Min Choi ◽  
Chang Hoon Lee ◽  
Chul Gyu Yoo ◽  
...  
Keyword(s):  
Interstitial Pneumonia ◽  
Secretory Protein ◽  
Idiopathic Interstitial Pneumonia ◽  
Clara Cell ◽  
Clara Cell Secretory Protein

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

IL-13-induced Clara cell secretory protein expression in airway epithelium: role of EGFR signaling pathway

2002 ◽  
Vol 283 (1) ◽  
pp. L67-L75 ◽  
Author(s):  
Suil Kim ◽  
Jae Jeong Shim ◽  
Pierre-Regis Burgel ◽  
Iris F. Ueki ◽  
Trang Dao-Pick ◽  
...  
Keyword(s):  
Growth Factor ◽  
Protein Expression ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Kinase Inhibitor ◽  
Growth Factor Receptor ◽  
Secretory Protein ◽  
Clara Cell ◽  
Clara Cell Secretory Protein ◽  
Gene And Protein Expression

Previous work showed that the Th2 cytokine interleukin (IL)-13 induces goblet cell metaplasia via an indirect mechanism involving the expression and subsequent activation of epidermal growth factor receptor (EGFR). Because Clara cell secretory protein (CCSP) expression has been reported in cells that express mucins, we examined the effect of IL-13 on CCSP gene and protein expression in pathogen-free rat airways and in pulmonary mucoepidermoid NCI-H292 cells. Intratracheal instillation of IL-13 induced CCSP mRNA in epithelial cells without cilia within 8–16 h, maximal between 24 and 48 h; CCSP immunostaining increased in a time-dependent fashion, maximal at 48 h. The CCSP immunostaining was localized in nongranulated secretory cells and goblet cells and in the lumen. Pretreatment with the selective EGFR tyrosine kinase inhibitor BIBX1522, cyclophosphamide (an inhibitor of bone marrow leukocyte mobilization), or a blocking antibody to IL-8 prevented CCSP staining. Treatment of NCI-H292 cells with the EGFR ligand transforming growth factor-α, but not with IL-13 alone, induced CCSP gene and protein expression. Selective EGFR tyrosine kinase inhibitors, BIBX1522 and AG1478, prevented CCSP expression in NCI-H292 cells, but the platelet-derived growth factor receptor tyrosine kinase inhibitor AG1295 had no effect. These findings indicate that IL-13 induces CCSP expression via an EGFR- and leukocyte-dependent pathway.

Clara cell secretory protein deficiency increases oxidant stress response in conducting airways

1998 ◽  
Vol 275 (2) ◽  
pp. L348-L356 ◽  
Author(s):  
Gregory W. Mango ◽  
Carl J. Johnston ◽  
Susan D. Reynolds ◽  
Jacob N. Finkelstein ◽  
Charles G. Plopper ◽  
...  
Keyword(s):  
Stress Response ◽  
Mrna Expression ◽  
Molecular Basis ◽  
Oxidant Stress ◽  
Secretory Protein ◽  
Protective Role ◽  
Clara Cell ◽  
Clara Cells ◽  
Clara Cell Secretory Protein ◽  
Oxidant Sensitivity

Little is known about the molecular basis for differential pulmonary oxidant sensitivity observed between genetically disparate members of the same species. We have generated mice that are deficient in Clara cell secretory protein (CCSP −/−) and that exhibit an oxidant-sensitive phenotype. We characterized the kinetics and distribution of altered stress-response [interleukin-6 (IL-6) and metallothionein (MT)] and epithelial cell-specific [cytochrome P-450 2F2 (CYP2F2)] gene expression to further understand the cellular and molecular basis for altered oxidant sensitivity in 129 strain CCSP −/− mice. Increases in IL-6 and MT mRNA abundance were detected by 2 h of exposure to 1 part/million ozone and preceded reductions in Clara cell CYP2F2 mRNA expression. Despite being qualitatively similar, increases in IL-6 and MT mRNA expression were enhanced in CCSP −/− mice with respect to coexposed 129 strain wild-type mice. Increased MT mRNA expression, indicative of the stress response, localized to the airway epithelium, surrounding mesenchyme, and endothelium of blood vessels. These results demonstrate a protective role for Clara cells and their secretions and indicate potential genetic mechanisms that may influence susceptibility to oxidant stress.

Lung Hyperpermeability, Clara-Cell Secretory Protein (CC16), and Susceptibility to Ozone of Five Inbred Strains of Mice

2003 ◽  
Vol 15 (12) ◽  
pp. 1209-1230 ◽  
Author(s):  
Fabrice Broeckaert ◽  
André Clippe ◽  
Ruddy Wattiez ◽  
Paul Falmagne ◽  
Alfred Bernard
Keyword(s):  
Inbred Strains ◽  
Secretory Protein ◽  
Clara Cell ◽  
Clara Cell Secretory Protein ◽  
Inbred Strains Of Mice

Serum Clara cell secretory protein (CC-16) in non-smoking patients with obstructive sleep apnea

2020 ◽  
Vol 24 (4) ◽  
pp. 1607-1612
Author(s):  
Ege Gulec Balbay ◽  
Ozlem Ataoglu ◽  
Merve Ercelik ◽  
Ibrahim Ethem Sahin ◽  
Ozlem Admis ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Secretory Protein ◽  
Clara Cell ◽  
Clara Cell Secretory Protein ◽  
Obstructive Sleep

Iroquoisgenes influence proximo-distal morphogenesis during rat lung development

2006 ◽  
Vol 290 (4) ◽  
pp. L777-L789 ◽  
Author(s):  
Minke van Tuyl ◽  
Jason Liu ◽  
Freek Groenman ◽  
Ross Ridsdale ◽  
Robin N. N. Han ◽  
...  
Keyword(s):  
Lung Development ◽  
Cell Formation ◽  
Surfactant Protein ◽  
Branching Morphogenesis ◽  
Secretory Protein ◽  
Clara Cell ◽  
Fgf Receptor ◽  
Clara Cell Secretory Protein ◽  
Morphogenetic Protein

Lung development is a highly regulated process directed by mesenchymal-epithelial interactions, which coordinate the temporal and spatial expression of multiple regulatory factors required for proper lung formation. The Iroquois homeobox ( Irx) genes have been implicated in the patterning and specification of several Drosophila and vertebrate organs, including the heart. Herein, we investigated whether the Irx genes play a role in lung morphogenesis. We found that Irx1– 3 and Irx5 expression was confined to the branching lung epithelium, whereas Irx4 was not expressed in the developing lung. Antisense knockdown of all pulmonary Irx genes together dramatically decreased distal branching morphogenesis and increased distention of the proximal tubules in vitro, which was accompanied by a reduction in surfactant protein C-positive epithelial cells and an increase in β-tubulin IV and Clara cell secretory protein positive epithelial structures. Transmission electron microscopy confirmed the proximal phenotype of the epithelial structures. Furthermore, antisense Irx knockdown resulted in loss of lung mesenchyme and abnormal smooth muscle cell formation. Expression of fibroblast growth factors (FGF) 1, 7, and 10, FGF receptor 2, bone morphogenetic protein 4, and Sonic hedgehog (Shh) were not altered in lung explants treated with antisense Irx oligonucleotides. All four Irx genes were expressed in Shh- and Gli2-deficient murine lungs. Collectively, these results suggest that Irx genes are involved in the regulation of proximo-distal morphogenesis of the developing lung but are likely not linked to the FGF, BMP, or Shh signaling pathways.

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