脑卒中归巢肽- dnase1通过选择性降解中性粒细胞胞外陷阱减轻肠缺血再灌注损伤。

IF 5.9 1区 生物学 Q2 CELL BIOLOGY
Tingting Liu, Xinrong Lv, Qingshan Xu, Xiuting Qi, Shenghui Qiu, Yaqi Luan, Na Shen, Jing Cheng, Lan Jin, Tian Tian, Wentao Liu, Lai Jin, Zhongzhi Jia
{"title":"脑卒中归巢肽- dnase1通过选择性降解中性粒细胞胞外陷阱减轻肠缺血再灌注损伤。","authors":"Tingting Liu, Xinrong Lv, Qingshan Xu, Xiuting Qi, Shenghui Qiu, Yaqi Luan, Na Shen, Jing Cheng, Lan Jin, Tian Tian, Wentao Liu, Lai Jin, Zhongzhi Jia","doi":"10.1111/cpr.70010","DOIUrl":null,"url":null,"abstract":"<p><p>Neutrophil extracellular traps (NETs) act as a vital first line of defence against tissue damage and pathogens, playing a significant role in improving diseases such as intestinal ischemia reperfusion injury (IRI). However, we observed that after intestinal injury, intestinal bacteria and lipopolysaccharides (LPS) can enter the circulatory system, leading to a significant secondary increase in NETs production and the subsequent activation of a coagulation cascade. This phenomenon contributes to a pathological process known as the 'second strike' of NETs, which exaggerates intestinal damage and microcirculation disturbance. Selectively mitigating the detrimental effects associated with this second strike presents a promising therapeutic strategy. We developed an innovative conjugate of stroke-homing peptide (SHp) and DNase1 (SHp-DNase1) to enhance the stability of DNase in the bloodstream while selectively targeting NETs in thromboembolic events. The effects of SHp-DNase1 on blood flow, ischemia, and vascular leakage were evaluated in a mouse model using laser Doppler flowmetry and an in vivo imaging system. Levels of LPS and NETs were elevated in patients with IRI. Similarly, the expression of NETs and LPS was upregulated in mice with intestinal IRI. In vivo imaging revealed disturbances in intestinal microcirculation, accompanied by intestinal leakage, which were effectively reversed by the administration of SHp-DNase1. Almost all of the SHp-DNase1 localised to the gastrointestinal tract, demonstrating the effective targeting of DNase1 to the site of intestinal injury via SHp guidance. Furthermore, the combination of SHp-DNase1 and CRO significantly reduced the expression of ischemia-inducible factors, leading to a marked decrease in mortality in the mouse model. These findings suggest that intestinal LPS leakage correlated with NETs exacerbation plays a critical role in IRI. The combination of SHp-DNase1 and CRO is an effective treatment strategy by simultaneously controlling inflammation and addressing microcirculatory disorders induced by NETs in the therapy of IRI.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70010"},"PeriodicalIF":5.9000,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Stroke-Homing Peptide-DNase1 Alleviates Intestinal Ischemia Reperfusion Injury by Selectively Degrading Neutrophil Extracellular Traps.\",\"authors\":\"Tingting Liu, Xinrong Lv, Qingshan Xu, Xiuting Qi, Shenghui Qiu, Yaqi Luan, Na Shen, Jing Cheng, Lan Jin, Tian Tian, Wentao Liu, Lai Jin, Zhongzhi Jia\",\"doi\":\"10.1111/cpr.70010\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Neutrophil extracellular traps (NETs) act as a vital first line of defence against tissue damage and pathogens, playing a significant role in improving diseases such as intestinal ischemia reperfusion injury (IRI). However, we observed that after intestinal injury, intestinal bacteria and lipopolysaccharides (LPS) can enter the circulatory system, leading to a significant secondary increase in NETs production and the subsequent activation of a coagulation cascade. This phenomenon contributes to a pathological process known as the 'second strike' of NETs, which exaggerates intestinal damage and microcirculation disturbance. Selectively mitigating the detrimental effects associated with this second strike presents a promising therapeutic strategy. We developed an innovative conjugate of stroke-homing peptide (SHp) and DNase1 (SHp-DNase1) to enhance the stability of DNase in the bloodstream while selectively targeting NETs in thromboembolic events. The effects of SHp-DNase1 on blood flow, ischemia, and vascular leakage were evaluated in a mouse model using laser Doppler flowmetry and an in vivo imaging system. Levels of LPS and NETs were elevated in patients with IRI. Similarly, the expression of NETs and LPS was upregulated in mice with intestinal IRI. In vivo imaging revealed disturbances in intestinal microcirculation, accompanied by intestinal leakage, which were effectively reversed by the administration of SHp-DNase1. Almost all of the SHp-DNase1 localised to the gastrointestinal tract, demonstrating the effective targeting of DNase1 to the site of intestinal injury via SHp guidance. Furthermore, the combination of SHp-DNase1 and CRO significantly reduced the expression of ischemia-inducible factors, leading to a marked decrease in mortality in the mouse model. These findings suggest that intestinal LPS leakage correlated with NETs exacerbation plays a critical role in IRI. The combination of SHp-DNase1 and CRO is an effective treatment strategy by simultaneously controlling inflammation and addressing microcirculatory disorders induced by NETs in the therapy of IRI.</p>\",\"PeriodicalId\":9760,\"journal\":{\"name\":\"Cell Proliferation\",\"volume\":\" \",\"pages\":\"e70010\"},\"PeriodicalIF\":5.9000,\"publicationDate\":\"2025-02-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Proliferation\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1111/cpr.70010\",\"RegionNum\":1,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Proliferation","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1111/cpr.70010","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

中性粒细胞胞外陷阱(NETs)是抵御组织损伤和病原体的重要第一道防线,在改善肠缺血再灌注损伤(IRI)等疾病中发挥着重要作用。然而,我们观察到,肠道损伤后,肠道细菌和脂多糖(LPS)可以进入循环系统,导致NETs产生的显着二次增加,随后激活凝血级联。这种现象导致了一种被称为NETs“二次发作”的病理过程,它会加剧肠道损伤和微循环障碍。选择性地减轻与第二次打击相关的有害影响是一种很有前途的治疗策略。我们开发了一种创新的卒中归巢肽(SHp)和DNase1 (SHp-DNase1)缀合物,以增强血液中dna酶的稳定性,同时选择性地靶向血栓栓塞事件中的NETs。采用激光多普勒血流仪和体内显像系统在小鼠模型中评估SHp-DNase1对血流、缺血和血管渗漏的影响。IRI患者的LPS和NETs水平升高。同样,在肠道IRI小鼠中,NETs和LPS的表达上调。体内成像显示肠道微循环紊乱,并伴有肠漏,可通过给予SHp-DNase1有效逆转。几乎所有的SHp-DNase1都定位于胃肠道,这表明通过SHp引导,DNase1可以有效地靶向肠道损伤部位。此外,SHp-DNase1与CRO联合使用可显著降低缺血诱导因子的表达,导致模型小鼠死亡率显著降低。这些发现表明,与NETs加重相关的肠道LPS渗漏在IRI中起关键作用。SHp-DNase1与CRO联合治疗是同时控制炎症和解决NETs诱导的微循环障碍的有效治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Stroke-Homing Peptide-DNase1 Alleviates Intestinal Ischemia Reperfusion Injury by Selectively Degrading Neutrophil Extracellular Traps.

Neutrophil extracellular traps (NETs) act as a vital first line of defence against tissue damage and pathogens, playing a significant role in improving diseases such as intestinal ischemia reperfusion injury (IRI). However, we observed that after intestinal injury, intestinal bacteria and lipopolysaccharides (LPS) can enter the circulatory system, leading to a significant secondary increase in NETs production and the subsequent activation of a coagulation cascade. This phenomenon contributes to a pathological process known as the 'second strike' of NETs, which exaggerates intestinal damage and microcirculation disturbance. Selectively mitigating the detrimental effects associated with this second strike presents a promising therapeutic strategy. We developed an innovative conjugate of stroke-homing peptide (SHp) and DNase1 (SHp-DNase1) to enhance the stability of DNase in the bloodstream while selectively targeting NETs in thromboembolic events. The effects of SHp-DNase1 on blood flow, ischemia, and vascular leakage were evaluated in a mouse model using laser Doppler flowmetry and an in vivo imaging system. Levels of LPS and NETs were elevated in patients with IRI. Similarly, the expression of NETs and LPS was upregulated in mice with intestinal IRI. In vivo imaging revealed disturbances in intestinal microcirculation, accompanied by intestinal leakage, which were effectively reversed by the administration of SHp-DNase1. Almost all of the SHp-DNase1 localised to the gastrointestinal tract, demonstrating the effective targeting of DNase1 to the site of intestinal injury via SHp guidance. Furthermore, the combination of SHp-DNase1 and CRO significantly reduced the expression of ischemia-inducible factors, leading to a marked decrease in mortality in the mouse model. These findings suggest that intestinal LPS leakage correlated with NETs exacerbation plays a critical role in IRI. The combination of SHp-DNase1 and CRO is an effective treatment strategy by simultaneously controlling inflammation and addressing microcirculatory disorders induced by NETs in the therapy of IRI.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Cell Proliferation
Cell Proliferation 生物-细胞生物学
CiteScore
14.80
自引率
2.40%
发文量
198
审稿时长
1 months
期刊介绍: Cell Proliferation Focus: Devoted to studies into all aspects of cell proliferation and differentiation. Covers normal and abnormal states. Explores control systems and mechanisms at various levels: inter- and intracellular, molecular, and genetic. Investigates modification by and interactions with chemical and physical agents. Includes mathematical modeling and the development of new techniques. Publication Content: Original research papers Invited review articles Book reviews Letters commenting on previously published papers and/or topics of general interest By organizing the information in this manner, readers can quickly grasp the scope, focus, and publication content of Cell Proliferation.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信