Cellular Expression and Functional Role of Bst-1 in the Kidney

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Cellular Expression and Functional Role of Bst-1 in the Kidney

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Co-author 1

Yasuna Nakamura ys-nakamura@nagasaki-u.ac.jp Nagasaki University Department of Physiology of Visceral Function and Body Fluid, Graduate School of Biomedical Sciences Nagasaki Japan *

Co-author 2

Ryusuke Umene rumene@nagasaki-u.ac.jp Nagasaki University Department of Physiology of Visceral Function and Body Fluid, Graduate School of Biomedical Sciences Nagasaki Japan -

Co-author 3

Tsuyoshi Inoue ts-inoue@nagasaki-u.ac.jp Nagasaki University Department of Physiology of Visceral Function and Body Fluid, Graduate School of Biomedical Sciences Nagasaki Japan -

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Introduction

We previously reported that bone marrow stromal cell antigen-1 (Bst-1) contributes to renal fibrosis, a key factor in the progression of chronic kidney disease. Furthermore, we demonstrated that Bst-1 deficiency attenuates renal injury after ischemia-reperfusion. However, the localization of Bst-1 in the kidney and its detailed mechanisms remain unclear.This study aimed to elucidate the cellular localization of Bst-1 in the kidney and to explore its potential renoprotective mechanisms using a sepsis-induced acute kidney injury (AKI) model.

Methods

Male Bst-1 knockout (KO) and wild-type (WT) mice aged 8–12 weeks were intraperitoneally injected with lipopolysaccharide (LPS) to induce septic AKI. Kidneys were harvested 24 hours after LPS administration to assess renal injury. To identify Bst-1–expressing cells, WT kidneys were dissociated into single-cell suspensions, and Bst-1–positive cells were isolated by flow cytometry, followed by single-cell RNA sequencing (scRNA-seq). Based on scRNA-seq findings, endothelial and macrophage cell lines expressing Bst-1 were used to evaluate the function of Bst-1 under LPS-induced stress.

Results

After LPS administration, WT mice showed significant increases in the renal injury markers Ngal and Kim-1, whereas these increases were suppressed in Bst-1 KO mice. scRNA-seq analysis revealed that Bst-1 was expressed in renal endothelial cells and macrophages. In vitro, Bst-1 knockdown in endothelial cells enhanced permeability, while in macrophages it reduced inflammatory responses.

Conclusion

Bst-1 deficiency attenuates renal injury in sepsis-induced AKI. These findings suggest that the renoprotective effect of Bst-1 deficiency may be primarily mediated through its role in macrophages.

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