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转录组分析揭示了腹部分离症肺毛细血管和后毛细血管静脉之间基因表达的差异。

Transcriptomic Analysis Reveals Differential Expression of Genes between Lung Capillary and Post Capillary Venules in Abdominal Sepsis.

机构信息

Department of Clinical Sciences, Malmö, Section for Surgery, Lund University, 214 28 Malmö, Sweden.

出版信息

Int J Mol Sci. 2021 Sep 22;22(19):10181. doi: 10.3390/ijms221910181.

DOI:10.3390/ijms221910181
PMID:34638535
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8507973/
Abstract

Lung endothelial cell dysfunction plays a central role in septic-induced lung injury. We hypothesized that endothelial cell subsets, capillary endothelial cells (capEC) and post capillary venules (PCV), might play different roles in regulating important pathophysiology in sepsis. In order to reveal global transcriptomic changes in endothelial cell subsets during sepsis, we induced sepsis in C57BL/6 mice by cecal ligation and puncture (CLP). We confirmed that CLP induced systemic and lung inflammation in our model. Endothelial cells (ECs) from lung capillary and PCV were isolated by cell sorting and transcriptomic changes were analyzed by bioinformatic tools. Our analysis revealed that lung capEC are transcriptionally different than PCV. Comparison of top differentially expressed genes (DEGs) of capEC and PCV revealed that capEC responses are different than PCV during sepsis. It was found that capEC are more enriched with genes related to regulation of coagulation, vascular permeability, wound healing and lipid metabolic processes after sepsis. In contrast, PCV are more enriched with genes related to chemotaxis, cell-cell adhesion by integrins, chemokine biosynthesis, regulation of actin filament process and neutrophil homeostasis after sepsis. In addition, we predicted some transcription factor targets that regulate a significant number of DEGs in sepsis. We proposed that targeting certain DEGs or transcriptional factors would be useful in protecting against sepsis-induced lung damage.

摘要

肺内皮细胞功能障碍在感染性休克引起的肺损伤中起核心作用。我们假设内皮细胞亚群，毛细血管内皮细胞（capEC）和后毛细血管小静脉（PCV），可能在调节感染性休克中的重要病理生理学方面发挥不同的作用。为了揭示感染性休克过程中内皮细胞亚群的全转录组变化，我们通过盲肠结扎和穿孔（CLP）在 C57BL/6 小鼠中诱导感染性休克。我们证实 CLP 在我们的模型中诱导了全身和肺部炎症。通过细胞分选分离肺毛细血管和 PCV 的内皮细胞，并通过生物信息学工具分析转录组变化。我们的分析表明，肺 capEC 的转录水平与 PCV 不同。capEC 和 PCV 的 top 差异表达基因（DEGs）的比较表明，capEC 在感染性休克期间的反应与 PCV 不同。发现在感染性休克后，capEC 中与凝血、血管通透性、伤口愈合和脂质代谢过程调节相关的基因更为丰富。相比之下，PCV 中与趋化作用、整合素介导的细胞-细胞粘附、趋化因子生物合成、肌动蛋白丝过程调节和中性粒细胞动态平衡相关的基因更为丰富。此外，我们预测了一些转录因子靶标，这些靶标调节感染性休克中大量的 DEGs。我们提出，针对某些 DEGs 或转录因子可能有助于防止感染性休克引起的肺损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7620/8507973/e74f2aedf681/ijms-22-10181-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7620/8507973/e74f2aedf681/ijms-22-10181-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7620/8507973/27f1070f85a6/ijms-22-10181-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7620/8507973/d4d8f342ef7f/ijms-22-10181-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7620/8507973/167071046744/ijms-22-10181-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7620/8507973/e74f2aedf681/ijms-22-10181-g007.jpg

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