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Article ; Online: High Mobility Group Proteins in Sepsis.

Liang, Guibin / He, Zhihui

2022 Volume 13, Page(s) 911152

Abstract: Sepsis, a systemic inflammatory response disease, is the most severe complication of infection and a deadly disease. High mobility group proteins (HMGs) are non-histone nuclear proteins binding nucleosomes and regulate chromosome architecture and gene ... ...

Abstract	Sepsis, a systemic inflammatory response disease, is the most severe complication of infection and a deadly disease. High mobility group proteins (HMGs) are non-histone nuclear proteins binding nucleosomes and regulate chromosome architecture and gene transcription, which act as a potent pro-inflammatory cytokine involved in the delayed endotoxin lethality and systemic inflammatory response. HMGs increase in serum and tissues during infection, especially in sepsis. A growing number of studies have demonstrated HMGs are not only cytokines which can mediate inflammation, but also potential therapeutic targets in sepsis. To reduce sepsis-related mortality, a better understanding of HMGs is essential. In this review, we described the structure and function of HMGs, summarized the definition, epidemiology and pathophysiology of sepsis, and discussed the HMGs-related mechanisms in sepsis from the perspectives of non-coding RNAs (microRNA, long non-coding RNA, circular RNA), programmed cell death (apoptosis, necroptosis and pyroptosis), drugs and other pathophysiological aspects to provide new targets and ideas for the diagnosis and treatment of sepsis.
MeSH term(s)	Cytokines/genetics ; High Mobility Group Proteins/genetics ; Humans ; Inflammation ; Nucleosomes ; Sepsis/metabolism
Chemical Substances	Cytokines ; High Mobility Group Proteins ; Nucleosomes
Language	English
Publishing date	2022-06-02
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.911152
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Article: Sepsis associated with acute lung injury over the period 2012-2021: a bibliometric analysis.

Liang, Guibin / Wang, Wenhua / He, Zhihui

Frontiers in physiology

2023 Volume 14, Page(s) 1079736

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2023-06-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2023.1079736
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Article ; Online: Cigarette smoke extract induces the senescence of endothelial progenitor cells by upregulating p300.

Liang, Guibin / He, Zhihui / Peng, Huaihuai / Zeng, Menghao / Zhang, Xuefeng

Tobacco induced diseases

2023 Volume 21, Page(s) 122

Abstract: 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 ... ...

Abstract	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.
Language	English
Publishing date	2023-10-03
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2194616-4
ISSN	1617-9625 ; 1617-9625
ISSN (online)	1617-9625
ISSN	1617-9625
DOI	10.18332/tid/170581
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Article ; Online: Screening of Sepsis Biomarkers Based on Bioinformatics Data Analysis.

Liang, Guibin / Li, Jiuang / Pu, Shiqian / He, Zhihui

Journal of healthcare engineering

2022 Volume 2022, Page(s) 6788569

Abstract: Methods: Gene expression profiles of GSE13904, GSE26378, GSE26440, GSE65682, and GSE69528 were obtained from the National Center for Biotechnology Information (NCBI). The differentially expressed genes (DEGs) were searched using limma software package. ... ...

Abstract	Methods: Gene expression profiles of GSE13904, GSE26378, GSE26440, GSE65682, and GSE69528 were obtained from the National Center for Biotechnology Information (NCBI). The differentially expressed genes (DEGs) were searched using limma software package. Gene Ontology (GO) functional analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and protein-protein interaction (PPI) network analysis were performed to elucidate molecular mechanisms of DEGs and screen hub genes. Results: A total of 108 DEGs were identified in the study, of which 67 were upregulated and 41 were downregulated. 15 superlative diagnostic biomarkers (CCL5, CCR7, CD2, CD27, CD274, CD3D, GNLY, GZMA, GZMH, GZMK, IL2RB, IL7R, ITK, KLRB1, and PRF1) for sepsis were identified by bioinformatics analysis. Conclusion: 15 hub genes (CCL5, CCR7, CD2, CD27, CD274, CD3D, GNLY, GZMA, GZMH, GZMK, IL2RB, IL7R, ITK, KLRB1, and PRF1) have been elucidated in this study, and these biomarkers may be helpful in the diagnosis and therapy of patients with sepsis.
MeSH term(s)	Biomarkers ; Computational Biology ; Data Analysis ; Gene Expression Profiling ; Gene Regulatory Networks ; Humans ; Receptors, CCR7 ; Sepsis/diagnosis ; Sepsis/genetics
Chemical Substances	Biomarkers ; Receptors, CCR7
Language	English
Publishing date	2022-09-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2545054-2
ISSN	2040-2309 ; 2040-2295
ISSN (online)	2040-2309
ISSN	2040-2295
DOI	10.1155/2022/6788569
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Article ; Online: Animal models of emphysema.

Liang, Gui-Bin / He, Zhi-Hui

Chinese medical journal

2019 Volume 132, Issue 20, Page(s) 2465–2475

Abstract: Objective: Chronic obstructive pulmonary disease (COPD) is a common chronic respiratory disease of human beings characterized by not fully reversible airflow limitation. Emphysema is the main pathological feature of COPD which causes high mortality ... ...

Abstract	Objective: Chronic obstructive pulmonary disease (COPD) is a common chronic respiratory disease of human beings characterized by not fully reversible airflow limitation. Emphysema is the main pathological feature of COPD which causes high mortality worldwide every year and consumes a large amount of medical expenses. This paper was to review the establishment and evaluation methods of animal models of emphysema or COPD, and put forward some new ideas on animal selection, method of modeling, and model evaluation. Data sources: The author retrieved information from the PubMed database up to July 2019, using various combinations of search terms, including emphysema, model, and animal. Study selection: Original articles, reviews, and other articles were searched and reviewed for animal models of emphysema. Results: This review summarized animal models of emphysema from the perspectives of animal selection, emphysema mechanism, modeling method and model evaluation, and found that passive smoking is the classic method for developing animal model of emphysema, mice are more suitable for experimental study on emphysema. Compared with pulmonary function indicators, airway inflammation indicators and oxidative stress indicators, pathomorphological indicators of lung tissue are the most important parameters for evaluating the establishment of the animal model of emphysema. Conclusions: Mice model induced by passive smoking is the classic animal model of emphysema. Pathomorphological indicators are the most important parameters for evaluating the establishment of the animal model of emphysema.
MeSH term(s)	Animals ; Disease Models, Animal ; Humans ; Inflammation/complications ; Pancreatic Elastase/physiology ; Pulmonary Disease, Chronic Obstructive/complications ; Pulmonary Emphysema/etiology ; Pulmonary Emphysema/genetics ; Pulmonary Emphysema/pathology ; Nicotiana/adverse effects ; Tobacco Smoke Pollution/adverse effects ; Vagus Nerve Stimulation
Chemical Substances	Tobacco Smoke Pollution ; Pancreatic Elastase (EC 3.4.21.36)
Language	English
Publishing date	2019-09-30
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	127089-8
ISSN	2542-5641 ; 0366-6999 ; 1002-0187
ISSN (online)	2542-5641
ISSN	0366-6999 ; 1002-0187
DOI	10.1097/CM9.0000000000000469
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Article ; Online: Endothelial progenitor cells systemic administration alleviates multi-organ senescence by down-regulating USP7/p300 pathway in chronic obstructive pulmonary disease.

Wang, Wenhua / Peng, Huaihuai / Zeng, Menghao / Liu, Jie / Liang, Guibin / He, Zhihui

Journal of translational medicine

2023 Volume 21, Issue 1, Page(s) 881

Abstract: Background: Chronic obstructive pulmonary disease (COPD) has impacted approximately 390 million people worldwide and the morbidity is increasing every year. However, due to the poor treatment efficacy of COPD, exploring novel treatment has become the ... ...

Abstract	Background: Chronic obstructive pulmonary disease (COPD) has impacted approximately 390 million people worldwide and the morbidity is increasing every year. However, due to the poor treatment efficacy of COPD, exploring novel treatment has become the hotpot of study on COPD. Endothelial progenitor cells (EPCs) aging is a possible molecular way for COPD development. We aimed to explore the effector whether intravenous administration of EPCs has therapeutic effects in COPD mice. Methods: COPD mice model was induced by cigarette smoke exposure and EPCs were injected intravenously to investigate their effects on COPD mice. At day 127, heart, liver, spleen, lung and kidney tissues of mice were harvested. The histological effects of EPCs intervention on multiple organs of COPD mice were detected by morphology assay. Quantitative real-time PCR and Western blotting were used to detect the effect of EPCs intervention on the expression of multi-organ senescence-related indicators. And we explored the effect of EPCs systematically intervening on senescence-related USP7/p300 pathway. Results: Compared with COPD group, senescence-associated β-galactosidase activity was decreased, protein and mRNA expression of p16 was down-regulated, while protein and mRNA expression of cyclin D1 and TERT were up-regulated of multiple organs, including lung, heart, liver, spleen and kidney in COPD mice after EPCs system intervention. But the morphological alterations of the tissues described above in COPD mice failed to be reversed. Mechanistically, EPCs systemic administration inhibited the expression of mRNA and protein of USP7 and p300 in multiple organs of COPD mice, exerting therapeutic effects. Conclusions: EPCs administration significantly inhibited the senescence of multiple organs in COPD mice via down-regulating USP7/p300 pathway, which presents a possibility of EPCs therapy for COPD.
MeSH term(s)	Animals ; Humans ; Mice ; Cellular Senescence ; Endothelial Progenitor Cells/pathology ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/therapy ; Pulmonary Disease, Chronic Obstructive/metabolism ; RNA, Messenger/metabolism ; Ubiquitin-Specific Peptidase 7/metabolism ; Signal Transduction ; Down-Regulation
Chemical Substances	RNA, Messenger ; Ubiquitin-Specific Peptidase 7 (EC 3.4.19.12)
Language	English
Publishing date	2023-12-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2118570-0
ISSN	1479-5876 ; 1479-5876
ISSN (online)	1479-5876
ISSN	1479-5876
DOI	10.1186/s12967-023-04735-x
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Article ; Online: Existence of multiple organ aging in animal model of emphysema induced by cigarette smoke extract.

Liang, Guibin / He, Zhihui / Chen, Yan / Zhang, Hongbo / Peng, Huaihuai / Zong, Dandan / Long, Yingjiao

Tobacco induced diseases

2022 Volume 20, Page(s) 2

Abstract: Introduction: It is commonly considered that COPD or at least emphysema represents accelerated lung aging induced in part by oxidative damage from cigarette smoke components. However, the issue if there are any aging signs in other organs in patients ... ...

Abstract	Introduction: It is commonly considered that COPD or at least emphysema represents accelerated lung aging induced in part by oxidative damage from cigarette smoke components. However, the issue if there are any aging signs in other organs in patients with COPD or emphysema remains unclear. The aim of this study is to explore whether there is multiple organ aging in the animal model of emphysema induced by cigarette smoke extract (CSE), and to ascertain the possible mechanisms, if any. Methods: The animal model of emphysema was induced by CSE. Histomorphological changes in lung, heart, liver, kidney and spleen tissues were measured after staining with hematoxylin and eosin (H&E). The concentrations of stem cell factor (SCF), CyclinD1 and superoxide dismutase (SOD) in serum were determined by ELISA kit. The expressions of p16 (INK4a), Sca-1, eNOS proteins and mRNA in lung, heart, liver, kidney and spleen tissues were detected by Western blotting and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), respectively. Decitabine (Dec) was applied to examine whether it could alter the changes caused by CSE. Results: The histomorphology of lung tissue was significantly changed, while other organs exhibited normal structure and histomorphology. The concentrations of SCF, CyclinD1 and SOD in serum were lower in the CSE group than in the control group. The expression levels of p16(INK4a) protein and mRNA in lung, heart, liver, kidney and spleen tissues were higher in the CSE group than in the control group, while the expression levels of Sca-1 and eNOS proteins and mRNA were lower in the CSE group than in the control group, in the tissues described above. Dec could partly alleviate the damages caused by CSE and the degree of alleviation resulted by Dec varied from organ to organ. Conclusions: In addition to the aging of the lung tissue in the emphysema animal model induced by CSE, the tissues of the heart, liver, kidney and spleen were also in the progress of aging, but the sensibility and affinity of lung to CSE were higher than those of the other organs. Multiple organ aging may also exist in the animal model of emphysema induced by CSE. DEC can partly alleviate the multiple organ aging caused by CSE.
Language	English
Publishing date	2022-01-17
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2194616-4
ISSN	1617-9625 ; 1617-9625
ISSN (online)	1617-9625
ISSN	1617-9625
DOI	10.18332/tid/143853
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Article ; Online: Cigarette smoke extract mediates cell premature senescence in chronic obstructive pulmonary disease patients by up-regulating USP7 to activate p300-p53/p21 pathway.

Zeng, Menghao / Zhang, Xuefeng / Xing, Wei / Wang, Qianlu / Liang, Guibin / He, Zhihui

Toxicology letters

2022 Volume 359, Page(s) 31–45

Abstract: Objectives: Tobacco hazard is one of the most severe public health issues in the world. It is believed that smoking is the most important factor leading to chronic obstructive pulmonary disease (COPD). Endothelial progenitor cells (EPCs) originate from ... ...

Abstract	Objectives: Tobacco hazard is one of the most severe public health issues in the world. It is believed that smoking is the most important factor leading to chronic obstructive pulmonary disease (COPD). Endothelial progenitor cells (EPCs) originate from the bone marrow and can effectively repair vascular endothelial damage and improve vascular endothelial function. Current studies suggest that EPCs senescence and EPCs depletion exist in smoking-related COPD, but the molecular mechanism remains unclear. Methods: Co-immunoprecipitation was used to detect the interaction between USP7 and p300. EPCs from smoking COPD patients were isolated, and the expressions of USP7 and p300 were detected by RT-PCR and Western Blot. Different concentrations of cigarette smoke extract (CSE) and USP7 or p300 inhibitors were used to treat EPCs, then the expression of p53, p53 target genes and aging-related genes were detected. Cell Counting Kit - 8 (CCK8) was used to detect cell proliferation, flow cytometry was used to detect cell cycle distribution, β-galactosidase (β-gal) staining and Lamp1 immunofluorescence was used to detect the proportion of aging cells. COPD mouse models were used to confirm the molecular mechanism. Results: USP7 and p300 interacted with each other, and USP7 affected the protein stability of p300 by regulating the ubiquitination of p300. There existed high expressions of USP7 and p300 proteins in EPCs of smoking COPD patients and COPD mouse model. CSE promoted the high expressions of USP7 and p300 in EPCs. Further studies showed that CSE mediated the USP7/p300-dependent high expression of p53 and activated the expression of p53 target genes especially p21. Activation of p53 - p21 pathway finally inhibited cell activity, led to cell cycle arrest and premature senescence of EPCs. Conclusion: CSE mediated up-regulation of USP7 and p300 activated p53 - p21 pathway was a molecular mechanism that might lead to COPD.
MeSH term(s)	Animals ; Cellular Senescence/drug effects ; Disease Models, Animal ; E1A-Associated p300 Protein/drug effects ; E1A-Associated p300 Protein/metabolism ; Endothelial Progenitor Cells/drug effects ; Endothelial Progenitor Cells/metabolism ; Healthy Volunteers ; Humans ; Metabolic Networks and Pathways/drug effects ; Mice ; Plant Extracts/therapeutic use ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Signal Transduction/drug effects ; Smoke ; Nicotiana/chemistry ; Tobacco Products ; Ubiquitin-Specific Peptidase 7/drug effects ; Ubiquitin-Specific Peptidase 7/metabolism
Chemical Substances	Plant Extracts ; Smoke ; E1A-Associated p300 Protein (EC 2.3.1.48) ; Ubiquitin-Specific Peptidase 7 (EC 3.4.19.12)
Language	English
Publishing date	2022-02-01
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article
ZDB-ID	433788-8
ISSN	1879-3169 ; 0378-4274
ISSN (online)	1879-3169
ISSN	0378-4274
DOI	10.1016/j.toxlet.2022.01.017
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Article ; Online: Discovery of 4-(N-dithiobenzyl piperazine)-1,8-naphthalimide as a potent multi-target antitumor agent with good efficacy, limited toxicity, and low resistance.

Liang, Si-Min / Liang, Gui-Bin / Wang, Hui-Ling / Jiang, Hong / Ma, Xian-Li / Wei, Jian-Hua / Huang, Ri-Zhen / Zhang, Ye

European journal of medicinal chemistry

2023 Volume 263, Page(s) 115937

Abstract: A series of 4-(N-dithiobenzyl piperazine)-1,8-naphthalimide derivatives 4-6 were designed, synthesized, and evaluated as novel multi-target antitumor agents. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) results showed that ... ...

Abstract	A series of 4-(N-dithiobenzyl piperazine)-1,8-naphthalimide derivatives 4-6 were designed, synthesized, and evaluated as novel multi-target antitumor agents. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) results showed that compounds 5j, 5k, and 6j exhibited superior in vitro antiproliferative activity in MGC-803, HepG-2, SKOV-3, and T24 cancer cell lines and the cisplatin-resistant cell line A549/DDP. HepG-2, SKOV-3, and T24 xenograft assay results revealed that compounds 5j, 5k, and 6j exhibited good antitumor effects compared with amonafide. The pathology results indicated that compound 5j exhibited the least comprehensive toxicity among the three compounds, identifying compound 5j as a good candidate antitumor agent with good efficacy, limited toxicity, and low resistance. Compound 5j was thus chose for further antitumor mechanism investigation. Results from the omics research, confocal immunofluorescence, Western blot, transmission electron microscopy, and flow cytometry indicated that compound 5j exerted antitumor effects through multiple mechanisms, including ferroptosis, autophagy, apoptosis, and cell cycle arrest. These results suggest that screening novel 1,8-naphthalimide-based antitumor agents for good efficacy, limited toxicity, and low resistance based on a multi-target drug strategy is feasible.
MeSH term(s)	Humans ; Naphthalimides/pharmacology ; Piperazine/pharmacology ; Cell Line, Tumor ; Drug Screening Assays, Antitumor ; Antineoplastic Agents/pharmacology ; Apoptosis ; Cell Proliferation
Chemical Substances	Naphthalimides ; Piperazine (1RTM4PAL0V) ; Antineoplastic Agents
Language	English
Publishing date	2023-11-10
Publishing country	France
Document type	Journal Article
ZDB-ID	188597-2
ISSN	1768-3254 ; 0009-4374 ; 0223-5234
ISSN (online)	1768-3254
ISSN	0009-4374 ; 0223-5234
DOI	10.1016/j.ejmech.2023.115937
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Article ; Online: p300/Sp1-Mediated High Expression of p16 Promotes Endothelial Progenitor Cell Senescence Leading to the Occurrence of Chronic Obstructive Pulmonary Disease.

He, Zhihui / Peng, Huaihuai / Gao, Min / Liang, Guibin / Zeng, Menghao / Zhang, Xuefeng

Mediators of inflammation

2021 Volume 2021, Page(s) 5599364

Abstract: Objective: Chronic obstructive pulmonary disease (COPD) is a common chronic disease and develops rapidly into a grave public health problem worldwide. However, what exactly causes the occurrence of COPD remains largely unclear. Here, we are trying to ... ...

Abstract	Objective: Chronic obstructive pulmonary disease (COPD) is a common chronic disease and develops rapidly into a grave public health problem worldwide. However, what exactly causes the occurrence of COPD remains largely unclear. Here, we are trying to explore whether the high expression of p16 mediated by p300/Sp1 can cause chronic obstructive pulmonary disease through promoting the senescence of endothelial progenitor cells (EPCs). Methods: Peripheral blood EPCs were isolated from nonsmoking non-COPD, smoking non-COPD, and smoking COPD patients. The expressions of p16, p300, and senescence-related genes were detected by RT-PCR and Western Blot. Then, we knocked down or overexpressed Sp1 and p300 and used the ChIP assay to detect the histone H4 acetylation level in the promoter region of p16, CCK8 to detect cell proliferation, flow cytometry to detect the cell cycle, and Results: The high expression of p16 was found in peripheral blood EPCs of COPD patients; the cigarette smoke extract (CSE) led to the increase of p16. The high expression of p16 in EPCs promoted cell cycle arrest and apoptosis. The CSE-mediated high expression of p16 promoted cell senescence. The expression of p300 was increased in peripheral blood EPCs of COPD patients. Moreover, p300/Sp1 enhanced the histone H4 acetylation level in the promoter region of p16, thereby mediating the senescence of EPCs. And knockdown of p300/Sp1 could rescue CSE-mediated cell senescence. Conclusion: p300/Sp1 enhanced the histone H4 acetylation level in the p16 promoter region to mediate the senescence of EPCs.
MeSH term(s)	Cell Proliferation/genetics ; Cellular Senescence/genetics ; Endothelial Progenitor Cells/metabolism ; Humans ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/metabolism ; Sp1 Transcription Factor/genetics ; Sp1 Transcription Factor/metabolism ; Nicotiana
Chemical Substances	Sp1 Transcription Factor ; SP1 protein, human
Language	English
Publishing date	2021-08-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2021/5599364
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