| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States; Department of Pulmonary Medicine, University of Debrecen, Debrecen, Hungary; Department of Pulmonary Medicine II, Josa Andras County Hospital, Nyiregyhaza, Hungary
2 Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
3 Division of Pulmonary Pharmacology, Research Center Borstel, 23845 Borstel, Germany
4 Department of Environmental and Occupational Health, University of Pittsburgh School of Public Health, Pittsburgh, Pennsylvania, United States
5 Department of Cell Biology and Physiology, University of Pittsburgh, PGH, Pennsylvania, United States
6 United States
* To whom correspondence should be addressed. E-mail: choiam{at}upmc.edu.
In the lungs, high-pressure mechanical ventilation induces an inflammatory response similar to that observed in acute respiratory distress syndrome. To further characterize these responses and to compare them to classical inflammatory pathways, we performed gene expression profiling analysis of 20,000 mouse genes in isolated blood-free (to exclude genes from sequestered leukocytes) perfused mouse lungs exposed to low-pressure ventilation (10 cm H2O), high-pressure ventilation (25 cm H2O, overventilation) and LPS-treatment. A large number of inflammatory and apoptotic genes was increased by both over ventilation and LPS. However, certain growth factor-related genes, as well as genes related to development, cellular communication and the cytoskeleton, were only regulated by over ventilation. We validated and confirmed increased mRNA expression pattern of 5 genes (amphiregulin, gravin, NUR77, CYR61, interleukin-11) by real time-polymerase chain reaction; furthermore, we confirmed increased protein expression of amphiregulin by immunohistochemistry and immunoblotting assays. These genes represent novel candidate genes in ventilator-induced lung injury.
This article has been cited by other articles:
|
|
 |
|
  S. Papaiahgari, A. Yerrapureddy, S. R. Reddy, N. M. Reddy, J. M. Dodd-O, M. T. Crow, D. N. Grigoryev, K. Barnes, R. M. Tuder, M. Yamamoto, et al. Genetic and Pharmacologic Evidence Links Oxidative Stress to Ventilator-induced Lung Injury in Mice Am. J. Respir. Crit. Care Med., December 15, 2007; 176(12): 1222 - 1235. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Dombrowsky and S. Uhlig Steroids and histone deacetylase in ventilation-induced gene transcription Eur. Respir. J., November 1, 2007; 30(5): 865 - 877. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Matute-Bello, M. M. Wurfel, J. S. Lee, D. R. Park, C. W. Frevert, D. K. Madtes, S. D. Shapiro, and T. R. Martin Essential Role of MMP-12 in Fas-Induced Lung Fibrosis Am. J. Respir. Cell Mol. Biol., August 1, 2007; 37(2): 210 - 221. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. M. Wurfel Microarray-based Analysis of Ventilator-induced Lung Injury Proceedings of the ATS, January 1, 2007; 4(1): 77 - 84. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
