The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Heme oxygenase-1 inhibits TNF-α-induced apoptosis in cultured fibroblasts
Abstract
Heme oxygenase (HO)-1 catalyzes the oxidative cleavage of heme to yield equimolar amounts of biliverdin, iron, and carbon monoxide. HO-1 is a stress response protein, the induction of which is associated with protection against oxidative stress. The mechanism(s) of protection is not completely elucidated, although it is suggested that one or more of the catalytic by-products provide antioxidant functions either directly or indirectly. The involvement of reactive oxygen species in apoptosis raised the question of a possible role for HO-1 in programmed cell death. Using the tetracycline-regulated expression system, we show here that conditional overexpression of HO-1 prevents tumor necrosis factor-α-induced apoptosis in murine L929 fibroblasts. Inhibition of apoptosis was not observed in the presence of tin protoporphyrin, a specific inhibitor of HO activity, and in cells overexpressing antisense HO-1. Interestingly, exogenous administration of a low concentration of carbon monoxide also prevented tumor necrosis factor-α-induced apoptosis in L929 fibroblasts. Inhibition of tumor necrosis factor-α-induced apoptosis by HO-1 overexpression was reversed by 1 H-(1,2,4)oxadiazolo(4,3- a)quinoxalin-1-one, an inhibitor of guanylate cyclase, which is a target enzyme for carbon monoxide. Taken together, our data suggest that the antiapoptotic effect of HO-1 may be mediated via carbon monoxide.
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Cites
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MethodPrevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked
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The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of Apoptosis
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WAF1/CIP1 is induced in p53-mediated G1 arrest and apoptosis.
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Mitogenic Signaling Mediated by Oxidants in Ras-Transformed Fibroblasts
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Self-citation
Cited by
Oxidative Stress: An Essential Factor in the Pathogenesis of Gastrointestinal Mucosal Diseases
Bhattacharyya, A., Chattopadhyay, R., Mitra, S., & Crowe, S. E. (2014) · Physiological Reviews · doi:10.1152/physrev.00040.2012 · Cited by 2,484
Systemic effects of chronic obstructive pulmonary disease
Agustí, A. G. N., Noguera, A., Sauleda, J., Sala, E., Pons, J., & Busquets, X. (2003) · European Respiratory Journal · doi:10.1183/09031936.03.00405703 · Cited by 1,045
Carbon Monoxide Generated by Heme Oxygenase 1 Suppresses Endothelial Cell Apoptosis
Brouard, S., Otterbein, L. E., Anrather, J., Tobiasch, E., Bach, F. H., Choi, A. M. K., & Soares, M. P. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.192.7.1015 · Cited by 984
Self-citationCarbon Monoxide: Endogenous Production, Physiological Functions, and Pharmacological Applications
Wu, L., & Wang, R. (2005) · Pharmacological Reviews · doi:10.1124/pr.57.4.3 · Cited by 962
Heme oxygenase: colors of defense against cellular stress
Otterbein, L. E., & Choi, A. M. K. (2000) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.2000.279.6.l1029 · Cited by 870
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Metadata
- Authors
- Petrache, I., Otterbein, L. E., Alam, J., Wiegand, G. W., & Choi, A. M. K.
- Venue
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Publisher
- American Physiological Society
- Published
- 2000-02-01
- Volume
- 278
- Issue
- 2
- Pages
- L312-L319
- ISSN
- 1040-0605 (ISSN-L)
- 1522-1504
- OpenAlex
- W2148308989
- Cited by
- 293
- References
- 41
- FWCI
- 7.77
- Type
- journal article
- Language
- en
- Open access
- closed
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