Renal ischemia and reperfusion impact the purinergic signaling in a vascular bed distant from the injured site

IF 3.3 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Jeferson Stabile , Raquel Silva Neres-Santos , Isabela Dorta Molina Hernandes , Carolina Victória Cruz Junho , Geovane Felippe Alves , Isabella Cardoso Silva , Marcela Sorelli Carneiro-Ramos , Cristina Ribas Fürstenau
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Abstract

Aims

Acute kidney injury (AKI) is a public health problem and represents a risk factor for cardiovascular diseases (CVD) and vascular damage. This study aimed to investigate the impact of AKI on purinergic components in mice aorta. Main methods: The kidney ischemia was achieved by the occlusion of the left kidney pedicle for 60 min, followed by reperfusion for 8 (IR8) and 15 (IR15) days. Renal function was assessed through biochemical assays, while gene expression levels were evaluated by RT-qPCR. Key findings: Analyses of renal parameters showed renal remodeling through mass loss in the left kidney and hypertrophy of the right kidney in the IR15 group. Furthermore, after 15 days, local inflammation was evidenced in the aorta. Moreover, the aorta purinergic components were significantly impacted by the renal ischemia and reperfusion model, with increases in gene expression of the pro-inflammatory purinoceptors P2Y1, P2Y2, P2Y6, and P2X4, potentially contributing to the vessel inflammation. The expression of NTPDase2 and ecto-5′-nucleotidase were also significantly increased in the aorta of the same group. In addition, both ATP and AMP hydrolysis were significantly increased in the aorta from IR15 animals, driving the entire purinergic cascade to the production of the anti-inflammatory adenosine. Significance: In short, this is the first time that inflammation of the aorta due to AKI was shown to have an impact on purinergic signaling components, with emphasis on the adenosinergic pathway. This seems to be closely implicated in the establishment of vascular inflammation in this model of AKI and deserves to be further investigated.

肾脏缺血和再灌注会影响远离受伤部位的血管床的嘌呤能信号传导。
目的:急性肾损伤(AKI)是一个公共卫生问题,也是心血管疾病(CVD)和血管损伤的一个危险因素。本研究旨在探讨急性肾损伤对小鼠主动脉嘌呤能成分的影响:主要方法:通过闭塞左肾蒂60分钟实现肾缺血,然后再灌注8天(IR8)和15天(IR15)。肾功能通过生化检测进行评估,基因表达水平通过 RT-qPCR 进行评估:主要研究结果:对肾脏参数的分析表明,IR15 组的肾脏重塑表现为左肾质量下降和右肾肥大。此外,15 天后,主动脉出现局部炎症。此外,肾缺血再灌注模型对主动脉嘌呤能成分有显著影响,促炎性嘌呤受体P2Y1、P2Y2、P2Y6和P2X4的基因表达增加,可能导致血管炎症。同组主动脉中 NTPDase2 和外-5'-核苷酸酶的表达也显著增加。此外,IR15 动物主动脉中的 ATP 和 AMP 水解均显著增加,推动整个嘌呤能级联产生抗炎腺苷:简而言之,这是首次证明 AKI 引起的主动脉炎症会影响嘌呤能信号转导成分,重点是腺苷能途径。这似乎与这种 AKI 模型中血管炎症的形成密切相关,值得进一步研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Biochimie
Biochimie 生物-生化与分子生物学
CiteScore
7.20
自引率
2.60%
发文量
219
审稿时长
40 days
期刊介绍: Biochimie publishes original research articles, short communications, review articles, graphical reviews, mini-reviews, and hypotheses in the broad areas of biology, including biochemistry, enzymology, molecular and cell biology, metabolic regulation, genetics, immunology, microbiology, structural biology, genomics, proteomics, and molecular mechanisms of disease. Biochimie publishes exclusively in English. Articles are subject to peer review, and must satisfy the requirements of originality, high scientific integrity and general interest to a broad range of readers. Submissions that are judged to be of sound scientific and technical quality but do not fully satisfy the requirements for publication in Biochimie may benefit from a transfer service to a more suitable journal within the same subject area.
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