Nicotine Inhibits Apoptosis and Stimulates Proliferation in Aortic Smooth Muscle Cells Through a Functional Nicotinic Acetylcholine Receptor
| العنوان: | Nicotine Inhibits Apoptosis and Stimulates Proliferation in Aortic Smooth Muscle Cells Through a Functional Nicotinic Acetylcholine Receptor |
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| المؤلفون: | Pierpaolo Coluccia, Andrea Fuso, Antonino Cavallaro, Alessandra Cucina |
| المصدر: | Journal of Surgical Research. 150:227-235 |
| بيانات النشر: | Elsevier BV, 2008. |
| سنة النشر: | 2008 |
| مصطلحات موضوعية: | Programmed cell death, medicine.medical_specialty, medicine.medical_treatment, Myocytes, Smooth Muscle, Basic fibroblast growth factor, Enzyme-Linked Immunosorbent Assay, Receptors, Nicotinic, Biology, Polymerase Chain Reaction, Nicotine, chemistry.chemical_compound, Internal medicine, medicine, Animals, Nicotinic Agonists, RNA, Messenger, Annexin A5, nicotinic acetylcholine receptor, Cells, Cultured, Cell Proliferation, Fluorescent Dyes, Neointimal hyperplasia, Growth factor, apoptosis, Bungarotoxins, musculoskeletal system, medicine.disease, smooth muscle cells, Cell biology, Fibroblast Growth Factors, Nicotinic acetylcholine receptor, Nicotinic agonist, Endocrinology, chemistry, nicotine, atherosclerosis, Dactinomycin, cardiovascular system, Cattle, Surgery, Signal Transduction, Transforming growth factor, medicine.drug |
| الوصف: | Atherosclerosis and neointimal hyperplasia formation are induced by alterations in the homeostatic balance between cell growth and cell death. Apoptosis is a physiological cell death process that, when deregulated, may be involved in many pathological conditions. Cigarette smoking is a primary risk factor for vascular disease and nicotine seems to exert its atherogenic effects in part through the increase of smooth muscle cell (SMC) proliferation. The aim of this study was to investigate the effect of nicotine on SMC apoptosis. Nicotine added for 24 and 72 h to serum deprived cell cultures resulted in a decrease of apoptotic SMCs. The inhibition was direct and not mediated by platelet-derived growth factor, basic fibroblast growth factor, and transforming growth factor beta(1), autocrinally released by nicotine-treated SMCs, because it was not influenced by addition of specific neutralizing antibodies. Apoptosis inhibition as well as the proliferation increase, and basic fibroblast growth factor expression on nicotine-treated SMCs were blocked by nicotinic acetylcholine receptor antagonists, including alpha-bungarotoxin, a competitive antagonist of alpha subunits of nicotinic receptor. In conclusion, we propose that nicotine could lead to the increase of neointimal SMCs in vascular lesions by inducing the inhibition of physiological SMC apoptosis and the increase of SMC proliferation. We also showed that nicotine signaling occurs as a result of activation of the classical nicotine receptor pathways. |
| تدمد: | 0022-4804 |
| DOI: | 10.1016/j.jss.2007.10.019 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0a6670383fb286411baf9846cdf43d8c https://doi.org/10.1016/j.jss.2007.10.019 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....0a6670383fb286411baf9846cdf43d8c |
| قاعدة البيانات: | OpenAIRE |
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