| pubmed-article:19116364 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19116364 | lifeskim:mentions | umls-concept:C0003947 | lld:lifeskim |
| pubmed-article:19116364 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:19116364 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
| pubmed-article:19116364 | lifeskim:mentions | umls-concept:C0033640 | lld:lifeskim |
| pubmed-article:19116364 | lifeskim:mentions | umls-concept:C1366765 | lld:lifeskim |
| pubmed-article:19116364 | lifeskim:mentions | umls-concept:C1367731 | lld:lifeskim |
| pubmed-article:19116364 | lifeskim:mentions | umls-concept:C0258823 | lld:lifeskim |
| pubmed-article:19116364 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:19116364 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:19116364 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:19116364 | pubmed:dateCreated | 2009-1-23 | lld:pubmed |
| pubmed-article:19116364 | pubmed:abstractText | Inhalation of asbestos and oxidant-generating pollutants causes injury and compensatory proliferation of lung epithelium, but the signaling mechanisms that lead to these responses are unclear. We hypothesized that a protein kinase (PK)Cdelta-dependent PKD pathway was able to regulate downstream mitogen-activated protein kinases, affecting pro- and anti-apoptotic responses to asbestos. Elevated levels of phosphorylated PKD (p-PKD) were observed in distal bronchiolar epithelial cells of mice inhaling asbestos. In contrast, PKCdelta-/- mice showed significantly lower levels of p-PKD in lung homogenates and in situ after asbestos inhalation. In a murine lung epithelial cell line, asbestos caused significant increases in the phosphorylation of PKCdelta-dependent PKD, ERK1/2, and JNK1/2/c-Jun that occurred with decreases in the BH3-only pro-apoptotic protein, Bim. Silencing of PKCdelta, PKD, and use of small molecule inhibitors linked the ERK1/2 pathway to the prevention of Bim-associated apoptosis as well as the JNK1/2/c-Jun pathway to the induction of apoptosis. Our studies are the first to show that asbestos induces PKD phosphorylation in lung epithelial cells both in vivo and in vitro. PKCdelta-dependent PKD phosphorylation by asbestos is causally linked to a cellular pathway that involves the phosphorylation of both ERK1/2 and JNK1/2, which play opposing roles in the apoptotic response induced by asbestos. | lld:pubmed |
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| pubmed-article:19116364 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19116364 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19116364 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:19116364 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19116364 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19116364 | pubmed:month | Feb | lld:pubmed |
