The Authors utilized an in vitro model in which HUVEC (human umbilical cord endothelial cells) were exposed to tobacco vapor/ in HEPES buffer to assess the role of tobacco constituents in causing cardiovascular disease. In the presence of Platelet-poor-plasma, C1q Complement protein deposition was significantly increased in the presence of tobacco vapor, regardless of nicotine content.
Ancell antibodies were used in EIA to assess levels of CD35, CD55 and CD59 molecules, which are known regulators of Complement deposition. CD35 expression was significantly up regulated in the presence of tobacco vapor regardless of nicotine content.
