The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
ET-1 stimulates pulmonary arterial smooth muscle cell proliferation via induction of reactive oxygen species
Abstract
Recent studies implicate reactive oxygen species (ROS) such as superoxide anions and H 2 O 2 in the proliferation of systemic vascular smooth muscle cells (SMCs). However, the role of ROS in SMC proliferation within the pulmonary circulation remains unclear. We investigated the effects of endothelin-1 (ET-1), a potential SMC mitogen, on ROS production and proliferation of fetal pulmonary artery SMCs (FPASMCs). Exposure to ET-1 resulted in increases in superoxide production and viable FPASMCs after 72 h. These increases were prevented by pretreatment with PD-156707. Treatment with pertussis toxin blocked the effects of ET-1, whereas cholera toxin stimulated superoxide production and increased viable cell numbers even in the absence of ET-1. Wortmannin, LY-294002, diphenyleneiodonium (DPI), 4-(2-aminoethyl)benzenesulfonyl fluoride, and apocynin also prevented the ET-1-mediated increases in superoxide production and viable cell numbers. Exposure to H 2 O 2 or diethyldithiocarbamate increased viable cell number by 37% and 50%, respectively. Conversely, ascorbic acid and DPI decreased viable cell number, which appeared to be due to an increase in programmed cell death. Our data suggest that ET-1 exerts a mitogenic effect on FPASMCs via an increase in ROS production and that antioxidants can block this effect via induction of apoptosis. Antioxidant treatment may therefore represent a potential therapy for pulmonary vascular diseases.
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Cited by
Pulmonary Arterial Hypertension: The Clinical Syndrome
Lai, Y.-C., Potoka, K. C., Champion, H. C., Mora, A. L., & Gladwin, M. T. (2014) · Circulation Research · doi:10.1161/circresaha.115.301146 · Cited by 402
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Molecular and cellular basis of pulmonary vascular remodeling in pulmonary hypertension
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Metadata
- Authors
- Wedgwood, S., Dettman, R. W., & Black, S. M.
- Venue
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Publisher
- American Physiological Society
- Published
- 2001-11-01
- Volume
- 281
- Issue
- 5
- Pages
- L1058-L1067
- ISSN
- 1040-0605 (ISSN-L)
- 1522-1504
- OpenAlex
- W2341635912
- Cited by
- 258
- References
- 32
- FWCI
- 6.08
- Type
- journal article
- Language
- en
- Open access
- closed
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