Macrophage polarization involved the inflammation of chronic obstructive pulmonary disease by S1P/HDAC1 signaling

被引:1
|
作者
Zhang, Min [1 ]
Hei, Ruoxuan [2 ]
Zhou, Zhou [3 ]
Xiao, Wendi [1 ]
Liu, Xi [1 ]
Chen, Yanwei [1 ,4 ]
机构
[1] Shenzhen Univ, Affiliated Hosp 1, Dept Nephrol, Shenzhen 518035, Guangdong, Peoples R China
[2] Air Force Mil Med Univ, Affiliated Hosp 2, Dept Clin Diag, 569 Xinsi Rd, Xian 710038, Shaanxi, Peoples R China
[3] Southern Univ Sci & Technol Hosp, Dept Pulm & Crit Care Med, Shenzhen 518102, Guangdong, Peoples R China
[4] Air Force Mil Med Univ, Affiliated Hosp 2, Dept Pulm & Crit Care Med, 569 Xinsi Rd, Xian 710038, Shaanxi, Peoples R China
来源
AMERICAN JOURNAL OF CANCER RESEARCH | 2023年 / 13卷 / 09期
基金
中国国家自然科学基金;
关键词
Chronic obstructive pulmonary disease; S1P; HDAC; macrophages; inflammation; HISTONE DEACETYLASE ACTIVITY; SPHINGOSINE; 1-PHOSPHATE; LUNG-FUNCTION; ANTIINFLAMMATORY ACTIVITY; SYSTEMIC INFLAMMATION; COPD PATIENTS; SPHINGOSINE-1-PHOSPHATE; EXACERBATION; RISK; MODULATION;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Globally, chronic obstructive pulmonary disease (COPD) is the cause of high morbidity and mortality, and constitutes a huge public health burden. Previous studies have reported that inflammation is closely related to COPD, but its potential mechanism is still unclear. Since the polarization of macrophages is involved in regulating inflammation, we assume that COPD changes the polarization of macrophages. To verify this, we investigated the relationship between the expression of S1PR1, HADC1, and inflammatory macrophages in COPD patients via flow cytometry, qRT-PCR, and western blot analysis. We found that macrophages of COPD individuals differentiated into M1 phenotype, and the expression of S1PR1 increased and HDAC1 decreased. S1PR1 also inhibits the expression of HDAC1, so S1PR1/HDAC1 signal regulates the polarization of macrophages. The results of the study put forward new ideas of the pathogenesis of COPD, and also proposed the possible treatment options.
引用
收藏
页码:4478 / 4489
页数:12
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