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

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...

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Autores principales: Liang, Guibin, He, Zhihui, Peng, Huaihuai, Zeng, Menghao, Zhang, Xuefeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: European Publishing on behalf of the International Society for the Prevention of Tobacco Induced Diseases (ISPTID) 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10546488/
https://www.ncbi.nlm.nih.gov/pubmed/37794858
http://dx.doi.org/10.18332/tid/170581
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author Liang, Guibin
He, Zhihui
Peng, Huaihuai
Zeng, Menghao
Zhang, Xuefeng
author_facet Liang, Guibin
He, Zhihui
Peng, Huaihuai
Zeng, Menghao
Zhang, Xuefeng
author_sort Liang, Guibin
collection PubMed
description 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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spelling pubmed-105464882023-10-04 Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300 Liang, Guibin He, Zhihui Peng, Huaihuai Zeng, Menghao Zhang, Xuefeng Tob Induc Dis Research Paper 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. European Publishing on behalf of the International Society for the Prevention of Tobacco Induced Diseases (ISPTID) 2023-10-03 /pmc/articles/PMC10546488/ /pubmed/37794858 http://dx.doi.org/10.18332/tid/170581 Text en © 2023 Liang G. et al. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License.
spellingShingle Research Paper
Liang, Guibin
He, Zhihui
Peng, Huaihuai
Zeng, Menghao
Zhang, Xuefeng
Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300
title Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300
title_full Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300
title_fullStr Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300
title_full_unstemmed Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300
title_short Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300
title_sort cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10546488/
https://www.ncbi.nlm.nih.gov/pubmed/37794858
http://dx.doi.org/10.18332/tid/170581
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