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.I have no potential conflict of interest to disclose.I did not use generative AI and AI-assisted technologies in the writing process.
Nakamura et al. (Wed,) studied this question.