Cigarette smoke extract affects methylation status and attenuates Sca-1 expression of mouse endothelial progenitor cell &lt;i&gt;in vitro&lt;/i&gt;

He, Zhijun; Chen, Yan; Chen, Ping; Xie, Li; Liang, Gongping; Zhang, Hongliang; Peng, Huaihuai

doi:10.18332/tid/131625

Cited by 3 publications

(2 citation statements)

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“…As in a method previously described, EPCs were derived from bone marrow of mouse 9 . First, the bones of mice were isolated after euthanasia, and mononuclear cells were isolated from bone marrow.…”

Section: Methodsmentioning

confidence: 99%

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Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300

Liang,

He,

Peng

et al. 2023

Tob. Induc. Dis.

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INTRODUCTION Endothelial progenitor cells (EPCs) are the main source of endothelial cells. The senescence of EPCs is involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoke extract (CSE) can directly induce the dysfunction and increased expression of senescence-related markers in EPCs cultured in vitro. Histone acetyltransferase p300 is a transcriptional activator, and its changes can lead to cell senescence. The present study investigated whether CSE can induce the senescence of EPCs by upregulating p300. METHODS EPCs were isolated from bone marrow of C57BL/6J mice by density gradient centrifugation. The p300 inhibitor C646 and agonist CTPB were used to interfere with EPCs, cell cycle and apoptosis were detected by flow cytometry, the proportion of senile cells was counted by β-galactosidase staining, the protein expression of p300, H4K12, Cyclin D1, TERT and Ki67 were detected by western blot. RESULTS Compared with the control group, the cell cycle of CSE group and CTPB group were blocked, the apoptosis rate and early apoptosis rate were increased, the proportion of senile cells counted by β-galactosidase staining was increased, the expression of p300 and H4K12 protein were increased, the expression of Cyclin D1, TERT and Ki67 protein were decreased. C646 could partly alleviate the damages caused by CSE. CONCLUSIONS CSE may promote the apoptosis and senescence of EPCs by upregulating the expression of p300 and H4K12 protein, thus preventing the transition of EPCs from G1 phase to S phase, affecting telomerase synthesis, and reducing EPCs proliferation.

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Section: Methodsmentioning

confidence: 99%

“…According to a previously published method, CSE was prepared 9 . A cigarette is prepared into 20 mL CSE stock solution.…”

Section: Methodsmentioning

confidence: 99%

Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300

Liang,

He,

Peng

et al. 2023

Tob. Induc. Dis.

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Recent advances in molecular biology of metabolic syndrome pathophysiology: endothelial dysfunction as a potential therapeutic target

Marzoog

2022

J Diabetes Metab Disord

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Current advances in molecular pathobiology of endotheliocytes dysfunctions are promising in finding the pathogenetic links to the emergence of insulin resistance syndrome. Physiologically, human organism homeostasis is strictly controlled to maintain metabolic processes at the acquainted level. Many factors are involved in maintaining these physiological processes in the organism and any deviation is undoubtedly accompanied by specific pathologies related to the affected process. Fortunately, the body’s defense system can solve and compensate for the impaired function through its multi-level defense mechanisms. The endothelium is essential in maintaining this homeostasis through its ability to modulate the metabolic processes of the organism. Pathological activity or impairment of physiological endothelium function seems directly correlated to the emergence of metabolic syndrome. The most accepted hypothesis is that endothelium distribution is due to endoplasmic reticulum stress and unfolded protein response development, which includes inhibition of long non-coding RNAs expression, cytokines disbalance, Apelin dysregulation, glycocalyx degradation, and specific microparticles. Clinically, the enhancement or restoration of normal endothelial cells can be a target for novel therapeutic strategies since the distribution of its physiological activity impairs homeostasis and results in the progression of metabolic syndrome, and induction of its physiological activity can ameliorate insulin resistance syndrome. Novel insights on the molecular mechanisms of endothelial cell dysfunction are concisely represented in this paper to enhance the present therapeutic tactics and advance the research forward to find new therapeutic targets.

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Modified Risk Tobacco Products and Cardiovascular Repair: Still Very “Smoky”

Cozzolino

Picchio

Floris

et al. 2023

CSCR

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Smoking habits represent a cardiovascular risk factor with tremendous impact on health. Other than damaging differentiated and functional cells of the cardiovascular system, they also negatively affect reparative mechanisms, such as those involved in cardiac fibrosis and in endothelial progenitor cell (EPC) activation. In recent years, alternative smoking devices, dubbed modified tobacco risk products (MRPs), have been introduced, but their precise impact on human health is still under evaluation. Also, they have not been characterized yet about the possible negative effects on cardiovascular reparative and regenerative cells, such as EPCs or pluripotent stem cells. In this perspective, we critically review the still scarce available data on the effects of MRPs on molecular and cellular mechanisms of cardiovascular repair and regeneration.

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Cigarette smoke extract affects methylation status and attenuates Sca-1 expression of mouse endothelial progenitor cell <i>in vitro</i>

Cited by 3 publications

References 51 publications

Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300

Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300

Recent advances in molecular biology of metabolic syndrome pathophysiology: endothelial dysfunction as a potential therapeutic target

Modified Risk Tobacco Products and Cardiovascular Repair: Still Very “Smoky”

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