The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Lung endothelial monocyte-activating protein 2 is a mediator of cigarette smoke-induced emphysema in mice.
Matthias Clauss; Robert Voswinckel; Gangaraju Rajashekhar; Ninotchka L Sigua; Heinz Fehrenbach; Natalia I Rush; Kelly S Schweitzer; Ali Ö Yildirim; Krzysztof Kamocki; Amanda J Fisher; et al. (Profiled Authors: Walter Hubbard; Rubin Tuder)
Indiana Center for Vascular Biology and Medicine and Department of Cellular and Integrative Physiology, Indiana University, Indianapolis, Indiana 46202, USA.
The Journal of clinical investigation 2011;121(6):2470-9.
Pulmonary emphysema is a disease characterized by alveolar cellular loss and inflammation. Recently, excessive apoptosis of structural alveolar cells has emerged as a major mechanism in the development of emphysema. Here, we investigated the proapoptotic and monocyte chemoattractant cytokine endothelial monocyte-activating protein 2 (EMAPII). Lung-specific overexpression of EMAPII in mice caused simplification of alveolar structures, apoptosis, and macrophage accumulation, compared with that in control transgenic mice. Additionally, in a mouse model of cigarette smoke-induced (CS-induced) emphysema, EMAPII levels were significantly increased in murine lungs. This upregulation was necessary for emphysema development, as neutralizing antibodies to EMAPII resulted in reduced alveolar cell apoptosis, inflammation, and emphysema-associated structural changes in alveoli and small airways and improved lung function. The mechanism of EMAPII upregulation involved an apoptosis-dependent feed-forward loop, since caspase-3 instillation in the lung markedly increased EMAPII expression, while caspase inhibition decreased its production, even in transgenic EMAPII mice. These findings may have clinical significance, as both current smokers and ex-smoker chronic obstructive pulmonary disease (COPD) patients had increased levels of secreted EMAPII in the bronchoalveolar lavage fluid compared with that of nonsmokers. In conclusion, we suggest that EMAPII perpetuates the mechanism of CS-induced lung emphysema in mice and, given its secretory nature, is a suitable target for neutralization antibody therapy.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
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Rubin M Tuder; Lijie Zhen; Chung Y Cho; Laima Taraseviciene-Stewart; Yasunori Kasahara; Daniela Salvemini; Norbert F Voelkel; Sonia C FloresAmerican journal of respiratory cell and molecular biology 2003;29(1):88-97.
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