The immune response to arterial damage in a mouse model of intermittent hypoxia: a transcriptomics analysis

The immune response to arterial damage in a mouse model of intermittent hypoxia: a transcriptomics analysis
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DOI:
10.1007/s11325-023-02866-5
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发表时间:
2023-06
影响因子:
2.5
通讯作者:
Chong Xu;Xiang-yun Cheng;Xiaoting Wang;Weijun Huang;Yupu Liu;H. Ye;J. Guan;Jinhong Shen;H. Yi
Chong Xu;Xiang-yun Cheng;Xiaoting Wang;Weijun Huang;Yupu Liu;H. Ye;J. Guan;Jinhong Shen;H. Yi
中科院分区:
医学4区
文献类型:
--
作者:
Chong Xu;Xiang-yun Cheng;Xiaoting Wang;Weijun Huang;Yupu Liu;H. Ye;J. Guan;Jinhong Shen;H. Yi

文献摘要

相似文献

目的间歇性低氧(IH)可导致小鼠动脉损伤甚至动脉粥样硬化,但IH致动脉损伤的具体机制尚不清楚。因此,本研究旨在阐明IH与动脉损伤之间的潜在机制。材料和方法利用RNA测序技术分析正常氧和IH小鼠胸主动脉的差异基因表达。此外,还进行了GO、KEGG途径和CiberSort分析。为了验证受IH影响的候选基因的表达,我们进行了定量RT-qPCR(qRT-PCR)。免疫组织化学(IHC)染色显示胸主动脉有免疫细胞浸润。结果IH组小鼠主动脉内中膜增厚,纤维结构紊乱。转录组学分析表明,在主动脉中,1137个上调基因和707个下调基因受到IH的影响,它们与免疫系统的激活和细胞的黏附密切相关。结论IH可能通过激活免疫反应、增强细胞黏附作用而导致主动脉结构的改变。
PurposeMice can develop arterial damage and even atherosclerosis under intermittent hypoxia (IH); however, the specific mechanism of arterial damage induced by IH remains unclear. Hence, this research aimed to illustrate the underlying mechanism linking IH to arterial injury.Materials and methodsThe differential gene expression of the thoracic aorta under normoxia or IH mice was analyzed utilizing RNA sequencing. Furthermore, GO, KEGG pathway, and CIBERSORT analyses were carried out. For verification of the expression of candidate genes affected by IH, quantitative RT-qPCR (qRT-PCR) was conducted. Immunohistochemical (IHC) staining revealed immune cell infiltration in the thoracic aorta.ResultsThe thickness of the intima-media of the mouse aorta was increased, and the fiber structure was disordered under IH. Transcriptomics analysis showed that in the aorta, 1137 upregulated genes and 707 downregulated genes were affected by IH, significantly related to the activation of the immune system and cell adhesion. Furthermore, B cell infiltration around the aorta was observed under IH.ConclusionsIH might lead to structural changes in the aorta by activating the immune response and enhancing cell adhesion.