ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Heme oxygenase-1-mediated autophagy protects against pulmonary endothelial cell death and development of emphysema in cadmium-treated mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
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- Cadmium toxicity and autophagy: a review.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
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- Heme Oxygenase-1 Is Involved in the Repair of Oxidative Damage Induced by Oxidized Fish Oil inMarine drugs · 2023Article
- Associations between environmental heavy metals exposure and preserved ratio impaired spirometry in the U.S. adults.Environmental science and pollution research international · 2023Article
- CEACAM6: A Novel Marker of Chronic Obstructive Pulmonary Disease Susceptibility?American journal of respiratory and critical care medicine · 2023Article
- Contribution of adaptive immunity to human COPD and experimental models of emphysema.Physiological reviews · 2023Review
- Role of cannabinoids and the endocannabinoid system in modulation of diabetic cardiomyopathy.World journal of diabetes · 2022Review
- Cadmium exposure enhances VE-cadherin expression in endothelial cells via suppression of ROCK signaling.Experimental and therapeutic medicine · 2022Article
- Fibrinogen mediates cadmium-induced macrophage activation and serves as a predictor of cadmium exposure in chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- p62 functions as a signal hub in metal carcinogenesis.Seminars in cancer biology · 2021Review
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- NETosis in the pathogenesis of acute lung injury following cutaneous chemical burns.JCI insight · 2021Article
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- Moderate Fluid Shear Stress Regulates Heme Oxygenase-1 Expression to Promote Autophagy and ECM Homeostasis in the Nucleus Pulposus Cells.Frontiers in cell and developmental biology · 2020Article
- Endosomes and Autophagy: Regulators of Pulmonary Endothelial Cell Homeostasis in Health and Disease.Antioxidants & redox signaling · 2019Review
- Transient receptor potential melastatin 2-mediated heme oxygenase-1 has a role for bacterial clearance by regulating autophagy in peritoneal macrophages during polymicrobial sepsis.Innate immunity · 2019Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
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 the role of HO-1 in cadmium-induced emphysema in mice by analyzing histopathology, micro-computed tomography scans, and lung function tests. CdCl2-exposed HO-1(-/-) mice exhibited more severe emphysema compared with HO-1(+/+) or hHO-1BAC mice. Loss of pulmonary endothelial cells (PECs) from the alveolar capillary membrane is recognized to be a target in emphysema. PECs from HO-1(+/+), HO-1(-/-), and hHO-1BAC were employed to define the underlying molecular mechanism for the protection from emphysema by HO-1. Electron microscopy, expression of autophagic markers (microtubule-associated protein 1B-light chain 3 II, autophagy protein 5, and Beclin1) and apoptotic marker (cleaved caspase 3) suggested induction of autophagy and apoptosis in PECs after CdCl2 treatment. CdCl2-treated HO-1(-/-) PECs exhibited downregulation of autophagic markers and significantly increased cleaved caspase 3 expression and activity (∼4-fold higher). Moreover, hHO-1BAC PECs demonstrated upregulated autophagy and absence of cleaved caspase 3 expression or activity. Pretreatment of HO-1(+/+) PECs with rapamycin induced autophagy and resulted in reduced cell death upon cadmium treatment. Induction of autophagy following CdCl2 treatment was found to be protective from apoptotic cell death. HO-1 induced protective autophagy in PECs and mitigated cadmium-induced emphysema.
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