Effect of Cigarette Smoke Components on Vascular Smooth Muscle Cell Migration Toward Platelet-Derived Growth Factor BB

Yoshiyama, Shinji; Horinouchi, Takahiro; Miwa, Soichi; Wang, Hong‐Hui; Kohama, Kazuhiro; Nakamura, Akio

doi:10.1254/jphs.10283sc

Cited by 12 publications

(7 citation statements)

References 15 publications

(18 reference statements)

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“…Previous studies, including our studies, reported that nicotine promotes the chemotaxis and migration of mammalian VSMCs [28,29]. In addition, we reported that GBaSM-4 cells were promoted in their migratory ability after chronic exposure to nicotine [36]. Normally, the differentiated VSMC have contractile function, but do not migrate or proliferate.…”

Section: Remodeling Of Vascular Smooth Muscle By Nicotinesupporting

confidence: 55%

Effects of Nicotine Contained in Tobacco Mainstream Smoke on Vascular Smooth Muscle Cells

Nakamura¹

2018

Atherosclerosis - Yesterday, Today and Tomorrow

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Cigarette smoking is a known risk factor for arteriosclerosis. In atheromatous plaques, the accumulation of vascular smooth muscle cells (VSMCs) have a phenotype differing from that of their normal contractile type. Nicotine is a major pharmacological agent in cigarette smoke. However, any direct effect of nicotine on VSMCs remains uncertain. We investigated the changes in the expression levels of differentiation markers and activity of mitogen-activated protein kinases (MAPKs) after nicotine exposure for 48 h using human aorta primary smooth muscle cells (HVSMC) differentiated with transforming growth factor-β. The results indicated that HVSMC phenotype changed to a synthetic-like phenotype after nicotine exposure. Nicotine is a factor that can change the expression of differentiation marker proteins in VSMCs. Thus, we proposed that nicotine directly affects the migration of VSMCs from the tunica media to atheromatous plaques in the vascular intima by inducing the transformation from a contractile-type to a synthetic-like type, which occurs before the development of atheromatous plaques. Nicotine is contained in nicotine patches and gums for smoking cessation. There may also promote atheromatous plaque formation. We anticipate that determining this mechanism will lead to new means of preventing and treating plaque formation and development in arteriosclerosis.

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Section: Remodeling Of Vascular Smooth Muscle By Nicotinesupporting

confidence: 55%

Effects of Nicotine Contained in Tobacco Mainstream Smoke on Vascular Smooth Muscle Cells

Nakamura¹

2018

Atherosclerosis - Yesterday, Today and Tomorrow

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“…Nicotine has anti-inflammatory effects in ulcerative colitis and has been shown to decrease the release of interleukin 1β and TNF-α in alveolar macrophages [31-34]. In addition, nicotine promotes vascular SMC migration [35]. The components of CSE, including nicotine, can induce changes such cell proliferation, cell migration, TNF-α secretion, and contraction in many types of cells.…”

Section: Discussionmentioning

confidence: 99%

Cigarette Smoke Extract-induced Reduction in Migration and Contraction in Normal Human Bronchial Smooth Muscle Cells

Yoon

Park

Cho

et al. 2011

Korean J Physiol Pharmacol

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The proliferation, migration, cytokine release, and contraction of airway smooth muscle cells are key events in the airway remodeling process that occur in lung disease such as asthma, chronic obstruction pulmonary disease, and cancer. These events can be modulated by a number of factors, including cigarette smoke extract (CSE). CSE-induced alterations in the viability, migration, and contractile abilities of normal human airway cells remain unclear. This study investigated the effect of CSE on cell viability, migration, tumor necrosis factor (TNF)-α secretion, and contraction in normal human bronchial smooth muscle cells (HBSMCs). Treatment of HBSMCs with 10% CSE induced cell death, and the death was accompanied by the generation of reactive oxygen species (ROS). CSE-induced cell death was reduced by N-acetyl-l-cysteine (NAC), an ROS scavenger. In addition, CSE reduced the migration ability of HBSMCs by 75%. The combination of NAC with CSE blocked the CSE-induced reduction of cell migration. However, CSE had no effect on TNF-α secretion and NF-κB activation. CSE induced an increase in intracellular Ca2+ concentration in 64% of HBSMCs. CSE reduced the contractile ability of HBSMCs, and the ability was enhanced by NAC treatment. These results demonstrate that CSE treatment induces cell death and reduces migration and contraction by increasing ROS generation in normal HBSMCs. These results suggest that CSE may induce airway change through cell death and reduction in migration and contraction of normal HBSMCs.

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“…CS contains greater than 1014 free radicals, including reactive oxygen and reactive nitrogen species per puff, which impose a strong oxidative burden resulting in an oxidant/antioxidant imbalance (5). The relative content of mitochondrial DNA (mtDNA), the only organelle DNA in animal cells encoding 13 subunits of the mitochondrial respiratory chain (MRC) complexes, was significantly decreased in heavy smokers (6).…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Demethylation Treatment on Cigarette Smoke Extract–Induced Mouse Emphysema Model

et al. 2013

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Abstract. In the present study, we explored the effects of demethylation in a cigarette smoke extract (CSE)-induced mouse emphysema model. Animals were randomly assigned to the control group, CSE group, 5-aza-2′-deoxycytidine (AZA) group, and CSE+AZA group (n = 10 per group). The mitochondrial transcription factor A (mtTFA) promoter methylation increased over 4-fold in the CSE group compared with the control group, which was reversed by AZA. The mtTFA and the cytochrome c oxidase subunit II (COX II) mRNA and protein levels were decreased approximately 3-fold in the CSE group compared with the control group, which was largely restored by AZA. Histological analysis showed that the CSE group exhibited emphysema compared with the control, which was alleviated by AZA. In addition, CSE significantly induced lung cell apoptosis and decreased lung function and lung mitochondrial COX activity, which was mostly restored by AZA. In conclusion, we for the first time provide evidence that demethylation therapy with AZA can effectively improve emphysema, lung function, lung cell apoptosis, and lung mitochondrial COX activity in a CSE-induced mouse emphysema model, which adds fresh insight into the therapeutic potential of demethylating agents in the prevention and treatment of cigarette smokeinduced emphysema.

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Effect of Cigarette Smoke Components on Vascular Smooth Muscle Cell Migration Toward Platelet-Derived Growth Factor BB

Cited by 12 publications

References 15 publications

Effects of Nicotine Contained in Tobacco Mainstream Smoke on Vascular Smooth Muscle Cells

Effects of Nicotine Contained in Tobacco Mainstream Smoke on Vascular Smooth Muscle Cells

Cigarette Smoke Extract-induced Reduction in Migration and Contraction in Normal Human Bronchial Smooth Muscle Cells

Protective Effect of Demethylation Treatment on Cigarette Smoke Extract–Induced Mouse Emphysema Model

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