Cigarette Smoke Extract Stimulates Rat Pulmonary Artery Smooth Muscle Cell Proliferation via PKC-PDGFB Signaling

Xing, Aiping; Du, Yong; Hu, Xiaoyun; Xu, Jun‐Fa; Zhang, Huanping; Li, Yang; Nie, Xin

doi:10.1155/2012/534384

Cited by 16 publications

(11 citation statements)

References 35 publications

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“…Studies also evidenced that CSE induced apoptosis of human airway SMCs [ 43 , 44 ], human pulmonary endothelial cells [ 10 ], and vascular endothelial cells [ 45 ]. In controversy, Xing and his colleagues [ 46 ] reported that stimulation of rat pulmonary artery SMCs with CSE significantly increased cell proliferation and promoted cell cycle progression. Promotions of cell proliferations stimulated by CSE were also observed on bovine tracheal SMCs [ 47 ] and human aortic SMCs [ 3 ].…”

Section: Discussionmentioning

confidence: 99%

Dual Effects of Cigarette Smoke Extract on Proliferation of Endothelial Progenitor Cells and the Protective Effect of 5-aza-2′-deoxycytidine on EPCs against the Damage Caused by CSE

Chen

et al. 2014

BioMed Research International

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Cigarette smoke is a major public health problem associated with multitude of diseases, including pulmonary and vascular diseases. Endothelial progenitor cells (EPCs) contribute to neovascularization and play an important role in the development of these diseases. The effect of CSE on EPCs is seldom studied. The aim of the current study is to observe the effect of CSE on biological behavior of EPCs and, further, to search for potential candidate agent in protection of proliferation of EPCs against the damage caused by CSE exposure in vitro. Methods. The proliferations of EPCs isolated from bone marrow of C57BL/6J mice were assessed by MTT after incubating the EPCs with a series of concentrations of CSE (1.0%, 2.5%, 5.0%, and 10.0%) for different times (3, 6, and 24 hours) as well as with 1.0% CSE in presence of 5-AZA-CdR for 24 hours. Results. The proliferations of EPCs were significantly enhanced after 3 hours of exposure to concentrations of 1.0% and 2.5% CSE but depressed when exposed to concentrations of 5.0% and 10.0% CSE. Furthermore, the 5-AZA-CdR in concentrations of 2.0 μmol/L and 5.0 μmol/L partly protected against the depression of proliferation of EPCs caused by CSE exposure. Conclusions. The CSE showed dual effects on proliferation of EPCs isolated from mice. The 5-AZA-CdR partly protected the proliferation of EPCs against the damage caused by CSE exposure in vitro, suggesting that DNA methylation may be involved in the dysfunction of EPCs induced by CSE.

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Section: Discussionmentioning

confidence: 99%

Dual Effects of Cigarette Smoke Extract on Proliferation of Endothelial Progenitor Cells and the Protective Effect of 5-aza-2′-deoxycytidine on EPCs against the Damage Caused by CSE

Chen

et al. 2014

BioMed Research International

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“…Proliferation of smooth muscle cells seems to be mediated via activation of the platelet-derived growth factor-protein kinase C signaling cascade. 68,69 Furthermore, polycyclic aromatic hydrocarbons (part of the hydrophobic fraction of cigarette smoke) were shown to activate aryl hydrocarbon receptor, which induces iNOS, leading finally to intimal thickening. 70 Likewise, polycyclic aromatic hydrocarbon-activated aryl hydrocarbon receptors can induce the transcription of receptors for chemokines and adhesion molecule receptors for leukocytes, thus amplifying inflammatory signals on the vascular endothelium.…”

Section: Arterioscler Thromb Vasc Biol March 2014mentioning

confidence: 99%

Smoking and Cardiovascular Disease

Meßner

Bernhard

2014

ATVB

841

329

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Abstract-Smoking represents one of the most important preventable risk factors for the development of atherosclerosis. The present review aims at providing a comprehensive summary of published data from clinical and animal studies, as well as results of basic research on the proatherogenic effect of smoking. Extensive search and review of literature revealed a vast amount of data on the influence of cigarette smoke and its constituents on early atherogenesis, particularly on endothelial cells. Vascular dysfunction induced by smoking is initiated by reduced nitric oxide (NO) bioavailability and further by the increased expression of adhesion molecules and subsequent endothelial dysfunction. Smoking-induced increased adherence of platelets and macrophages provokes the development of a procoagulant and inflammatory environment. After transendothelial migration and activation, macrophages take up oxidized lipoproteins arising from oxidative modifications and transdifferentiate into foam cells. In addition to direct physical damage to endothelial cells, smoking induces tissue remodeling, and prothrombotic processes together with activation of systemic inflammatory signals, all of which contribute to atherogenic vessel wall changes. There are still great gaps in our knowledge about the effects of smoking on cardiovascular disease. However, we know that smoking cessation is the most effective measure for reversing damage that has already occurred and preventing fatal cardiovascular outcomes. Clinical DataEvidence for smoking-induced initial vascular damage and endothelial dysfunction stems from an array of clinical studies analyzing endothelial function using various techniques. 6 As mentioned above, in 1993, Celermajer et al 5 were able to show that continuous smoking impairs FMD of the brachial artery in a dose-dependent manner, shown by the strong association between FMD and pack years smoked. This was also found to be the case with coronary arteries in a study by Zeiher et al. 7 Interestingly, reduction of endothelium-dependent dilatation by smoking was reversible, and significant improvement of FMD 1 year after cessation has been reported. 8 Likewise, a recent study of Amato et al 9 revealed that smoking light cigarettes impairs FMD as much as smoking regular cigarettes, arguing against light cigarettes as a less harmful alternative.Measurement of FMD represents a useful tool to assess the effects of smoking on the vascular wall. Independent of its FMD reducing activity, smoking was shown to induce other proatherogenic alterations in the vascular wall (eg, by deposition of smoke chemicals). The time needed to restore interrupted functions of the vascular endothelium will depend on the specific process that has caused the endothelial damage; some alterations of the endothelial wall may vanish more rapidly than others, without these being reflected by improved FMD.Clinical studies assessing the interrelation of secondhand smoking and FMD reported strong correlations. Secondhand smoking was shown to impair endo...

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“…PDGF acts as a mitogen and chemoattractant for VSMCs and induces transition of the mature contractile VSMCs into a proliferative and secretory phenotype. Further, cigarette smoke induced PDGF- protein kinase C signalling has been shown to induce VSMC proliferation [79]. PDGF, via PDGF receptor beta (PDGFRβ), also induces STAT-1 signalling pathway that leads to disease progression.…”

Section: Modulation Of Vsmc Dynamics and Atherosclerosismentioning

confidence: 99%

Novel Insights in the Metabolic Syndrome-induced Oxidative Stress and Inflammation-mediated Atherosclerosis

Varghese

Patel

Yadav

2018

CCR

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Cigarette Smoke Extract Stimulates Rat Pulmonary Artery Smooth Muscle Cell Proliferation via PKC-PDGFB Signaling

Cited by 16 publications

References 35 publications

Dual Effects of Cigarette Smoke Extract on Proliferation of Endothelial Progenitor Cells and the Protective Effect of 5-aza-2′-deoxycytidine on EPCs against the Damage Caused by CSE

Dual Effects of Cigarette Smoke Extract on Proliferation of Endothelial Progenitor Cells and the Protective Effect of 5-aza-2′-deoxycytidine on EPCs against the Damage Caused by CSE

Smoking and Cardiovascular Disease

Novel Insights in the Metabolic Syndrome-induced Oxidative Stress and Inflammation-mediated Atherosclerosis

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