Heme oxygenase-1-mediated autophagy protects against pulmonary endothelial cell death and development of emphysema in cadmium-treated mice.

@article{Surolia2015HemeOA,
  title={Heme oxygenase-1-mediated autophagy protects against pulmonary endothelial cell death and development of emphysema in cadmium-treated mice.},
  author={R. Surolia and Suman Karki and Hyun-Kon Kim and Zhihong Yu and T. Kulkarni and S. Mirov and A. Carter and S. Rowe and S. Matalon and V. Thannickal and A. Agarwal and V. Antony},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2015},
  volume={309 3},
  pages={
          L280-92
        }
}
Pulmonary exposure to cadmium, a major component of cigarette smoke, has a dramatic impact on lung function and the development of emphysema. Cigarette smoke exposure induces heme oxygenase-1 (HO-1), a cytoprotective enzyme. In this study, we employed a truncated mouse model of emphysema by intratracheal instillation of cadmium (CdCl2) solution (0.025% per 1 mg/kg body wt) in HO-1(+/+), HO-1(-/-), and overexpressing humanized HO-1 bacterial artificial chromosome (hHO-1BAC) mice. We evaluated… Expand
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