Zhang Min, Hei Ruoxuan, Zhou Zhou, Xiao Wendi, Liu Xi, Chen Yanwei
Department of Pulmonary Critical Care Medicine, The 1st Affiliated Hospital of Shenzhen University Shenzhen 518035, Guangdong, PR China.
Department of Clinical Diagnose, The Second Affiliated Hospital of The Air Force Military Medical University No. 569 Xinsi Road, Xi'an 710038, Shaanxi, PR China.
Am J Cancer Res. 2023 Sep 15;13(9):4478-4489. eCollection 2023.
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.
在全球范围内,慢性阻塞性肺疾病(COPD)是高发病率和高死亡率的病因,构成了巨大的公共卫生负担。先前的研究报告称,炎症与COPD密切相关,但其潜在机制仍不清楚。由于巨噬细胞的极化参与调节炎症,我们推测COPD会改变巨噬细胞的极化。为了验证这一点,我们通过流式细胞术、qRT-PCR和蛋白质免疫印迹分析研究了COPD患者中S1PR1、HADC1的表达与炎性巨噬细胞之间的关系。我们发现,COPD患者的巨噬细胞分化为M1表型,S1PR1的表达增加而HDAC1的表达降低。S1PR1还抑制HDAC1的表达,因此S1PR1/HDAC1信号调节巨噬细胞的极化。该研究结果提出了COPD发病机制的新思路,也提出了可能的治疗选择。