Cigarette smoke extract induced rat pulmonary artery smooth muscle cells proliferation via PKCα-mediated cyclin D1 expression

Zeng, Daxiong; Xu, Yongjian; Liu, Xiansheng; Wang, Ran; Xiang, Min

doi:10.1002/jcb.23131

Cited by 15 publications

(12 citation statements)

References 46 publications

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“…Low concentrations of CSE (1, 2 and 5%) increased cell proliferation, while high concentrations exhibited a significant inhibition on cell proliferation. These results were in accordance with previous studies (34)(35)(36).…”

Section: Discussionsupporting

confidence: 94%

Inhibition of FHL1 inhibits cigarette smoke extract-induced proliferation in pulmonary arterial smooth muscle cells

Chen

et al. 2015

Molecular Medicine Reports

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Cigarette smoke can induce pulmonary vascular remodeling, which involves pulmonary artery smooth muscle cell (PASMC) proliferation, resulting in pulmonary hypertension in chronic obstructive pulmonary disease. FHL1 is a member of the FHL subfamily, characterized by an N‑terminal half LIM domain, followed by four complete LIM domains, and has been suggested to be critical in cell proliferation. However, the effects of FHL1 on cigarette smoke‑induced PASMC proliferation and the precise molecular mechanism remain to be elucidated. The present study demonstrated that the protein expression of FHL1 correlated with cigarette smoke extract (CSE)‑induced PASMC proliferation. Knockdown of the expression of FHL1 using siRNA significantly suppressed cell proliferation and inhibited the cell cycle transition between the G1 and S phase by regulating the cyclin‑dependent kinase pathway at the basal level and following CSE stimulation. By contrast, overexpressing FHL1 using an adenovirus increased cell proliferation and promoted the cell cycle transition between the G1 and S phase. Furthermore, CSE significantly increased the protein expression of FHL1, however, exerted no effect on the mRNA expression levels. This alteration was due to the prolonged FHL1 half‑life, leading to the antagonizing of protein degradation. Collectively, these data suggested that FHL1 may be involved in excessive cell proliferation and may represent a potential therapeutic target for pulmonary hypertension.

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Section: Discussionsupporting

confidence: 94%

Inhibition of FHL1 inhibits cigarette smoke extract-induced proliferation in pulmonary arterial smooth muscle cells

Chen

et al. 2015

Molecular Medicine Reports

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“…It has been demonstrated that intervention with anisodamine, an antagonist of muscarinic acetylcholine receptors, via increasing the expression of cyclin D1, prevents smoking-induced ASMC proliferation, exerting a protective and reversing effect regarding CSE-induced changes (27,28). It has been suggested that inhibition of four and a half LIM domains protein 1 limited the CSE-induced proliferation of pulmonary arterial SMCs and may represent a potential therapeutic target for pulmonary hypertension (19).…”

Section: Discussionmentioning

confidence: 99%

Cigarette smoke extract promotes proliferation of airway smooth muscle cells through suppressing C/EBP-α expression

Guan

Cai²,

et al. 2017

Experimental and Therapeutic Medicine

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Cigarette smoke has been considered a major contributor to the pathogenesis of chronic obstructive pulmonary disease (COPD). In COPD patients, the airway smooth muscle layer has been observed to be markedly thickened and the proliferation of airway smooth muscle cells (ASMCs) was therefore used by the present study as a model to assess the impact of cigarette smoke extract (CSE). ASMCs were exposed to various concentrations of CSE and the proliferation of the cells was analyzed by an MTT assay. Furthermore, the expression levels of calreticulin and CCAAT/enhancer-binding protein alpha (C/EBP-α) in CSE-stimulated ASMCs were determined by polymerase chain reaction and western blot analyses. In addition, the effects of RNA interference (RNAi) to knockdown calreticulin and/or C/EBP-α on ASMC proliferation were studied. CSE was found to promote the proliferation of ASMCs, which was associated with increased expression of calreticulin and decreased expression of C/EBP-α. Knockdown of calreticulin resulted in the upregulation of C/EBP-α and inhibition of cell proliferation, while simultaneous knockdown of C/EBP-α promoted cell proliferation. The present study revealed that CSE promoted the proliferation of ASMCs, which was mediated by inhibition of C/EBP-α. These findings shed new light on airway remodeling in COPD and may provide novel approaches for therapies.

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“…Finally, brief SHS exposure also has been shown to induce intimal smooth muscle cell proliferation, 98 promote early low-density lipoprotein oxidation, [99][100][101] and even may enhance monocyte adhesion to vascular endothelium. [102][103][104] These mechanisms, in addition to depressed endothelial cell progenitor activity and the resultant dysfunctional vascular repair also seen, 105 create a microenvironment conducive to enhanced atherosclerotic plaque formation.…”

Section: The Physiological Effects Of Shsmentioning

confidence: 99%

Second-Hand Tobacco Smoke and Cardiovascular Disease Risk

Dunbar

Gotsis

Frishman

2013

Cardiology in Review

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In this review, we have sought to examine the epidemiological, basic science, and public health data regarding the association between second-hand smoke (SHS) exposure and the development of coronary heart disease (CHD). SHS increases the risk of CHD by 25-30% according to multiple cohort, case-control, and meta-analytical studies. Physiologic and basic science research suggest that the mechanisms by which SHS affects the cardiovascular system are multiple and include increased thrombogenesis and low-density lipoprotein oxidation, decreased exercise tolerance, dysfunctional flow-mediated vasodilatation, and activation of inflammatory pathways with concomitant oxidative damage and impaired vascular repair. As a result, chronic exposure promotes atherogenesis and the development of cardiovascular disease, increasing the risk of having an acute coronary syndrome (ACS). With the implementation of statewide and nationwide public smoke-free legislation across the United States and Europe, respectively, over the last 10-15 years, there has been a significant and reciprocal decline in the incidence of emergency admissions for ACS by an average 17% despite persistent attempts on the part of the tobacco industry to diminish the correlation between SHS exposure and CHD. These findings underscore the importance of the effects of smoking legislation on community health.

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Cigarette smoke extract induced rat pulmonary artery smooth muscle cells proliferation via PKCα-mediated cyclin D1 expression

Cited by 15 publications

References 46 publications

Inhibition of FHL1 inhibits cigarette smoke extract-induced proliferation in pulmonary arterial smooth muscle cells

Inhibition of FHL1 inhibits cigarette smoke extract-induced proliferation in pulmonary arterial smooth muscle cells

Cigarette smoke extract promotes proliferation of airway smooth muscle cells through suppressing C/EBP-α expression

Second-Hand Tobacco Smoke and Cardiovascular Disease Risk

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