Bone marrow stromal cell antigen-1 deficiency protects from acute kidney injury

Author:

Inoue Tsuyoshi12ORCID,Umene Ryusuke23,Sung Sun-Sang J.1ORCID,Tanaka Shinji1,Huang Liping1,Yao Junlan1,Hashimoto Noritatsu2,Wu Chia-Hsien2,Nakamura Yasuna2ORCID,Nishino Tomoya3,Ye Hong1,Rosin Diane L.4ORCID,Ishihara Katsuhiko5ORCID,Okusa Mark D.1ORCID

Affiliation:

1. Division of Nephrology, Center for Immunity, Inflammation, and Regenerative Medicine, University of Virginia, Charlottesville, Virginia, United States

2. Department of Physiology of Visceral Function and Body Fluid, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan

3. Department of Nephrology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan

4. Department of Pharmacology, University of Virginia, Charlottesville, Virginia, United States

5. Department of Design for Medical and Health Care, Faculty of Health and Welfare Services Administration, Kawasaki University of Medical Welfare, Okayama, Japan

Abstract

Acute kidney injury (AKI), a serious disease for which there is no effective Federal Drug Administration-approved treatment, is associated with high mortality rates. Bone marrow stromal cell antigen-1 (Bst1) is a cell surface molecule that can cause kidney fibrosis, but its role in AKI is largely unknown. Our study showed that Bst1−/− mice revealed a protective effect against renal bilateral ischemia-reperfusion injury (IRI). Adoptive transfer studies confirmed that Bst1 expression in hematopoietic cells, especially neutrophils, contributed to renal bilateral IRI.

Funder

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

MEXT | Japan Society for the Promotion of Science

Japan Agency for Medical Research and Development

MEXT | JST | Fusion Oriented REsearch for disruptive Science and Technology

Publisher

American Physiological Society

Subject

Physiology

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