title: Role of perivascular adipose tissue in nicotine‑induced endothelial cell inflammatory responses.
abstract: Smoking is considered to be one of the primary causes of atherosclerosis and vascular injury. Previous studies have shown that nicotine in tobacco can lead to vascular inflammation and endothelial dysfunction. Perivascular adipose tissue (PVAT) is known to secrete various types of adipokines to maintain vascular homeostasis. The present study investigated whether nicotine‑induced PVAT malfunction can accelerate endothelial inflammation and eventually lead to endothelial dysfunction. The levels of inflammatory adipokines, including nuclear factor (NF)‑κB, interleukin (IL)‑1β, IL‑6 and tumor necrosis factor (TNF)‑α, the ICAM‑1 and VCAM‑1 adhesion molecules and secretion of adiponectin were assessed in mature adipocytes and endothelial cells cultured alone or in co‑culture under nicotine stimulation. It was found that nicotine reduced the secretion of adiponectin and stimulated secretion of the NF‑κB, IL‑1β, IL‑6 and TNF‑α inflammatory adipokines in mature adipocytes. Although nicotine stimulated endothelial cells to secrete IL‑1β and IL‑6, no significant increase in the secretion of TNF‑α was observed. The co‑culture of mature adipocytes with endothelial cells markedly augmented the expression of the NF‑κB, IL‑1β, IL‑6 and TNF‑α inflammatory adipokines and the ICAM‑1 and VCAM‑1 adhesion molecules, and significantly lowered the levels of adiponectin. These findings suggested that nicotine induced mature adipocyte dysfunction, which caused the abnormal secretion of adiponectin and inflammatory adipokines, and exacerbated endothelial inflammation. These findings also suggested a mechanism whereby nicotine induced the secretion of adiponectin and inflammatory cytokines by adipocytes. The results of the present study elucidated a novel pathway induced by cigarette smoke, which contributed to atherosclerosis and vascular injury.
authors.affiliation: Department of Vascular Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, P.R. China.
authors.forename: Chao-Nan
authors.initials: CN
authors.lastname: Wang
authors.affiliation: Department of Vascular Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, P.R. China.
authors.forename: Gen-Huan
authors.initials: GH
authors.lastname: Yang
authors.affiliation: Department of Vascular Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, P.R. China.
authors.forename: Zhan-Qi
authors.initials: ZQ
authors.lastname: Wang
authors.affiliation: Department of Vascular Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, P.R. China.
authors.forename: Chang-Wei
authors.initials: CW
authors.lastname: Liu
authors.affiliation: Department of Vascular Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, P.R. China.
authors.forename: Tian-Jia
authors.initials: TJ
authors.lastname: Li
authors.affiliation: Department of Vascular Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, P.R. China.
authors.forename: Zhi-Chao
authors.initials: ZC
authors.lastname: Lai
authors.affiliation: State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, P.R. China.
authors.forename: Shi-Ying
authors.initials: SY
authors.lastname: Miao
authors.affiliation: State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, P.R. China.
authors.forename: Lin-Fang
authors.initials: LF
authors.lastname: Wang
authors.affiliation: Department of Vascular Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, P.R. China.
authors.forename: Bao
authors.initials: B
authors.lastname: Liu
mesh_terms: D017667:Adipocytes / Q000378:metabolism; D054392:Adipokines / Q000096:biosynthesis; D052242:Adiponectin / Q000096:biosynthesis; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D002450:Cell Communication; D002460:Cell Line; D016207:Cytokines / Q000096:biosynthesis; D042783:Endothelial Cells / Q000187:drug effects* / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D051379:Mice; D009538:Nicotine / Q000009:adverse effects*
chemical_list: D054392:Adipokines; D052242:Adiponectin; C499919:Adipoq protein, mouse; D015815:Cell Adhesion Molecules; D016207:Cytokines; D009538:Nicotine