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Note: For a complete listing of the lab's publications, click here to link out to the Pub Med publication search engine, and type in "Stripp, B". However, some of the notable lab publications are listed below. |
Publications in the past year:
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Giangreco A, Arwert EN, Rosewell IR, Snyder J, Watt FM, Stripp BR. Stem cells are dispensable for lung homeostasis but restore airways after injury. Proc. Natl. Acad. Sci. USA. (Epub 2009)
Snyder JC, Reynolds SD, Hollingsworth JW, Li Z, Kaminski N, Stripp BR. Clara cells attenuate the inflammatory response through regulation of macrophage behaviour. Am. J. Respir. Cell Mol. Biol. (Epub 2009)
Zemke, A.C., R. M. Teisanu, A. Giangreco, J. A. Drake, B. L. Brockway, S. D. Reynolds, and B. R. Stripp. Beta-catenin is not necessary for maintenance or repair of the bronchiolar epithelium. Am. J. Respir. Cell Mol. Biol. (Epub 2009).
Snyder JC, Teisanu RM, Stripp BR. Endogenous lung stem cells and contribution to disease. J Pathol. 2009;217:254-264.
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Selected Earlier Publications:
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Reynolds, S.D., Reynolds, P.R., Snyder, J.C., Whyte, F., Paavola, K.J., and Stripp, B.R. CCSP regulates cross talk between secretory cells and both ciliated cells and macrophages of the conducting airway. Am J Physiol Lung Cell Mol Physiol. 2007;293:L114-123. This study provides direct evidence that Clara cell dysfunction leads to biochemical changes within lung monocyte/macrophages.
Plopper, C.G., Mango, G.W., Hatch, G.E., Wong, V.J., Toskala, E., Reynolds, S.D., Tarkington, B.K., and Stripp, B.R. Elevation of susceptibility to ozone-induced acute tracheobronchial injury in transgenic mice deficient in Clara cell secretory protein. Toxicol Appl Pharmacol. 2006;213:74-85. This paper follows up on earlier work from this laboratory investigating roles for Clara cells in protection against oxidant lung pollutants such as ozone.
Hong, K.U., Reynolds, S.D., Watkins, S., Fuchs, E., and Stripp, B.R. In vivo differentiation potential of tracheal basal cells: evidence for multipotent and unipotent subpopulations. Am J Physiol Lung Cell Mol Physiol. 2004;286:L643-649. These papers were the first such studies in the lung to use a transgenic approach involving ligand-regulated Cre recombinase to define lineage relationships within basal cells of the repairing proximal airway.
This paper defined the broncho-alveolar duct junction (BADJ) as a microenvironment (stem cell niche) that maintains bronchiolar stem cells.
This paper was the first to define a microenvironment within the bronchiole that maintains local tissue stem cells.
This was the first use of transgenic mice for conditional cell ablation. We were able to demonstrate a critical role for CCSP-expressing cells in bronchiolar repair.
This paper described the first knock-out model of a lung-specific gene. This model allowed us to reveal functional roles for Clara cells in lung homeostasis.
In this paper we were able to reveal a unique pattern of airway repair following ablation of Clara cells that formed the basis for our evolving interest in bronchiolar stem cells and mechanisms of lung tissue repair.
In this paper we provided details of the gene structure of the mouse CCSP gene and defined promoter elements that have subsequently been used to drive expression of transgenes within airway secreotry cells.
This paper was one of the first to describe promoter elements of the rat CC10/CCSP gene that directed airway-specific gene expression in transgenic mice.
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