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Am J Physiol Lung Cell Mol Physiol (June 5, 2002). doi:10.1152/ajplung.00422.2001
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Articles in PresS, published online ahead of print June 5, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00422.2001
Submitted on October 30, 2001
Accepted on May 17, 2002

Inhibition of proteasome activity is involved in cobalt-induced apoptosis of human alveolar macrophages

Jun Araya1, Muneharu Maruyama1*, Akira Inoue1, Tadashi Fujita1, Junko Kawahara1, Kazuhiko Sassa1, Ryuji Hayashi1, Yukio Kawagishi1, Naohiro Yamashita1, Eiji Sugiyama1, and Masashi Kobayashi1

1 The First Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Toyama, Japan

* To whom correspondence should be addressed. E-mail: mmaruyam-tym{at}umin.ac.jp.

Inhalation of particulate cobalt has been known to induce interstitial lung disease. There is growing evidence that apoptosis plays a crucial role in physiological and pathological settings, and that ubiquitin-proteasome system is involved in the regulation of apoptosis. Cadmium, the same transitional heavy metal as cobalt, has been reported to accumulate ubiquitinated proteins in neuronal cells. Based on these findings, we hypothesized that cobalt would induce apoptosis in lung by the disturbance of ubiquitin-proteasome pathway. To evaluate this, we exposed U-937 cells and human alveolar macrophages (AMs) to cobalt chloride (CoCl2), and examined their apoptosis by DNA fragmentation assay, DAPI staining, and Western blot analysis. Cobalt chloride induced apoptosis and accumulated ubiquitinated proteins. Exposure to CoCl2 inhibited proteasome activity in U-937 cells. Cobalt-induced apoptosis was mediated via mitochondrial pathway because CoCl2 released cytochrome-c from mitochondria. These results suggest that cobalt-induced apoptosis of AMs may be one of the mechanisms for cobalt-induced lung injury, and that the accumulation of ubiquitinated proteins might be involved in this apoptotic process.




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