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ICAM-1 缺失延缓老年糖尿病小鼠的修复过程。

ICAM-1 deletion delays the repair process in aging diabetic mice.

机构信息

Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, PR China.

School of Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.

出版信息

Metabolism. 2021 Jan;114:154412. doi: 10.1016/j.metabol.2020.154412. Epub 2020 Oct 22.

DOI:10.1016/j.metabol.2020.154412
PMID:33164859
Abstract

BACKGROUND

The delayed repair process in the aging diabetic population is becoming an alarming public health concern. ICAM-1 plays an important role in orchestrating the repair process by mediating neutrophil recruitment and phagocytosis. However, little is known about the role of ICAM-1 in aging diabetic repair.

METHODS

By causing injury in aging diabetic mice with ICAM-1 deletion (AD-ICAM-1), we found that AD-ICAM-1 mice exhibited a delayed repair process with incomplete re-epithelialization and reduced angiogenesis. Additionally, high-throughput Illumina sequencing was performed to evaluate the microbiota of such mice.

RESULTS

The results indicate that the microbiota of the AD-ICAM-1 injury site differed taxonomically at both the phylum and genus levels. Neutrophil recruitment and phagocytic function were also reduced in the AD-ICAM-1 group. Notably, major inflammatory biomarker expression was also detected in AD-ICAM-1 injured tissue.

CONCLUSIONS

Overall, this study demonstrated that AD-ICAM-1 mice exhibit delayed repair. In addition, neutrophil recruitment and phagocytic activity were impaired in the AD-ICAM-1 group, which may have allowed microbes to colonize the injury site.

摘要

背景

老龄化糖尿病患者的延迟修复过程正成为一个令人担忧的公共卫生问题。ICAM-1 通过介导中性粒细胞募集和吞噬作用在协调修复过程中发挥重要作用。然而,关于 ICAM-1 在衰老糖尿病修复中的作用知之甚少。

方法

通过在具有 ICAM-1 缺失的衰老糖尿病小鼠(AD-ICAM-1)中造成损伤,我们发现 AD-ICAM-1 小鼠表现出延迟修复过程,表现为不完全的再上皮化和血管生成减少。此外,还进行了高通量 Illumina 测序以评估此类小鼠的微生物组。

结果

结果表明,AD-ICAM-1 损伤部位的微生物组在门和属水平上在分类上存在差异。AD-ICAM-1 组中的中性粒细胞募集和吞噬功能也降低。值得注意的是,在 AD-ICAM-1 损伤组织中也检测到主要炎症生物标志物的表达。

结论

总体而言,这项研究表明 AD-ICAM-1 小鼠表现出延迟修复。此外,AD-ICAM-1 组中的中性粒细胞募集和吞噬活性受损,这可能允许微生物定植于损伤部位。

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ICAM-1 deletion delays the repair process in aging diabetic mice.ICAM-1 缺失延缓老年糖尿病小鼠的修复过程。
Metabolism. 2021 Jan;114:154412. doi: 10.1016/j.metabol.2020.154412. Epub 2020 Oct 22.
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Increased expression of intercellular adhesion molecule-1 (ICAM-1) in diabetic rat glomeruli: glomerular hyperfiltration is a potential mechanism of ICAM-1 upregulation.糖尿病大鼠肾小球中细胞间黏附分子-1(ICAM-1)表达增加:肾小球高滤过是ICAM-1上调的潜在机制。
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Front Genet. 2020 Dec 18;11:616988. doi: 10.3389/fgene.2020.616988. eCollection 2020.