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Nicotinic and PDGF-receptor function are essential for nicotine-stimulated mitogenesis in human vascular smooth muscle cells by Ivo A. Pestana; Roberto I. Vazquez-Padron; Abdelouahab Aitouche; Si M. Pham is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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## Abstract Cigarette smoking is implicated in the formation of occlusive vascular diseases. Nicotine's role in this process is incompletely understood. Nicotine's effect on human aortic vascular smooth muscle cells (HaVSMC) and the role of the nicotinic receptor (nAChR), platelet‐derived growth factor (PDGF), and the PDGF‐receptor (PDGF‐R) in this response were studied. Nicotine's mitogenic effect was characterized by three methods: thymidine incorporation, a viability/proliferation assay based on metabolic conversion of tetrazolium salt to formazan dye and cell counting. Nicotine administration (10^−6^ M) stimulated cell cycle entry marked by increased DNA synthesis, PCNA and cyclin D1 production, and increased cell division. Nicotinic receptor blockade with d‐tubocurarine, a nicotinic AchR blocker, decreased nicotine‐induced DNA synthesis, and cell division (0.33 ± 0.04, 0.77 ± 0.31‐fold decrease, respectively). Nicotine increased cellular PDGF‐BB transcript levels and protein release (ELISA: 1.6 ± 0.5‐fold increase) but not PDGF‐AA or PDGF–AB release. Nicotine increased PDGFβ‐receptor protein content. PDGF inactivation with anti‐PDGF antibody abolished nicotine‐induced DNA synt

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Author

Ivo A. Pestana; Roberto I. Vazquez-Padron; Abdelouahab Aitouche; Si M. Pham

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0730-2312)

Published

2005

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)