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Authors: Möckel, Tamara
Boegel, Sebastian
Schwarting, Andreas
Title: Transcriptome analysis of renal ischemia/reperfusion (I/R) injury in BAFF and BAFF-R deficient mice
Online publication date: 19-Feb-2024
Year of first publication: 2023
Language: english
Abstract: Acute kidney injury (AKI) accompanies with high morbidity and mortality. Incomplete renal recovery can lead to chronic and finally end-stage kidney disease, which results in the requirement of lifelong dialysis or kidney transplantation. Consequently, finding predictive biomarker and therefore developing preventive therapeutic approaches is an urgent need. For this purpose, a better understanding of the mechanism underlying AKI is necessary. The cytokine BAFF (B cell activating factor) is related to AKI by supporting B cells, which in turn play an important role in inflammatory processes and the production of antibodies. In our study, we investigated the role of BAFF and its receptor BAFF-R in the early phase of AKI. Therefore, we performed the well-established ischemia/reperfusion (I/R) model in BAFF (B6.129S2-Tnfsf13btm1Msc/J) and BAFF-R (B6(Cg)-Tnfrsf13ctm1Mass/J) deficient mice. Transcriptome of ischemic and contralateral control kidneys was analyzed and compared to wildtype littermates. We detected the upregulation of Lcn2, Lyz2, Cd44, Fn1 and Il1rn in ischemic kidneys as well as the downregulation of Kl. Furthermore, we revealed different expression patterns in BAFF and BAFF-R knockout mice. Compared to wildtype littermates, up- and downregulation of each investigated gene were higher in BAFF-R knockout and lower in BAFF knockout. Our findings indicate a positive impact of BAFF knockout in early phase of AKI, while BAFF-R knockout seems to worsen I/R injury. In addition, our study shows for the first time a remarkable renal upregulation of Lyz2 in a murine I/R model. Therefore, we consider Lyz2 as conceivable predictive or early biomarker in case of I/R and AKI.
DDC: 610 Medizin
610 Medical sciences
Institution: Johannes Gutenberg-Universität Mainz
Department: FB 04 Medizin
Place: Mainz
Version: Published version
Publication type: Zeitschriftenaufsatz
Document type specification: Scientific article
License: CC BY
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Journal: PLOS ONE
Pages or article number: e0291619
Publisher: PLOS
Publisher place: San Francisco, California, US
Issue date: 2023
ISSN: 1932-6203
Publisher DOI: 10.1371/journal.pone.0291619
Appears in collections:DFG-491381577-G

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