Renoprotective effects of extracellular fibroblast specific protein 1 via nuclear factor erythroid 2-related factor-mediated antioxidant activity.

Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
18 Dec 2023
Historique:
received: 10 08 2023
accepted: 12 12 2023
medline: 19 12 2023
pubmed: 19 12 2023
entrez: 18 12 2023
Statut: epublish

Résumé

Podocyte expression of fibroblast specific protein 1 (FSP1) is observed in various types of human glomerulonephritis. Considering that FSP1 is secreted extracellularly and has been shown to have multiple biological effects on distant cells, we postulated that secreted FSP1 from podocytes might impact renal tubules. Our RNA microarray analysis in a tubular epithelial cell line (mProx) revealed that FSP1 induced the expression of heme oxygenase 1, sequestosome 1, solute carrier family 7, member 11, and cystathionine gamma-lyase, all of which are associated with nuclear factor erythroid 2-related factor (Nrf2) activation. Therefore, FSP1 is likely to exert cytoprotective effects through Nrf2-induced antioxidant activity. Moreover, in mProx, FSP1 facilitated Nrf2 translocation to the nucleus, increased levels of reduced glutathione, inhibited the production of reactive oxygen species (ROS), and reduced cisplatin-induced cell death. FSP1 also ameliorated acute tubular injury in mice with cisplatin nephrotoxicity, which is a representative model of ROS-mediated tissue injury. Similarly, in transgenic mice that express FSP1 specifically in podocytes, tubular injury associated with cisplatin nephrotoxicity was also mitigated. Extracellular FSP1 secreted from podocytes acts on downstream tubular cells, exerting renoprotective effects through Nrf2-mediated antioxidant activity. Consequently, podocytes and tubular epithelial cells have a remote communication network to limit injury.

Identifiants

DOI: 10.1038/s41598-023-49863-y PMID: 38110482
pubmed: 38110482
doi: 10.1038/s41598-023-49863-y
pii: 10.1038/s41598-023-49863-y
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

22540

Subventions

Organisme : Janan Society for the Promotion of Sciences
ID : JP18K08203
Organisme : Janan Society for the Promotion of Sciences
ID : JP20H03696
Organisme : Japan Society for the Promotion of Science
ID : JP15H04836

Informations de copyright

© 2023. The Author(s).

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Auteurs

Naoki Takahashi (N)

Department of Nephrology, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuokashimoaizuki, Eiheiji-Cho, Yoshida-Gun, Fukui, 910-1193, Japan.

Seiji Yokoi (S)

Department of Nephrology, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuokashimoaizuki, Eiheiji-Cho, Yoshida-Gun, Fukui, 910-1193, Japan.

Hideki Kimura (H)

Department of Clinical Laboratory, Faculty of Medical Sciences, University of Fukui, Fukui, Japan.

Hironobu Naiki (H)

Department of Molecular Pathology, Faculty of Medical Sciences, University of Fukui, Fukui, Japan.

Taiji Matsusaka (T)

Institute of Medical Sciences and Department of Basic Medicine, Tokai University School of Medicine, Kanagawa, Japan.

Yasuhiko Yamamoto (Y)

Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.

Kimihiko Nakatani (K)

Department of Nephrology, Yamashiro General Medical Center, Kizugawa, Kyoto, Japan.

Kenji Kasuno (K)

Department of Nephrology, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuokashimoaizuki, Eiheiji-Cho, Yoshida-Gun, Fukui, 910-1193, Japan.

Masayuki Iwano (M)

Department of Nephrology, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuokashimoaizuki, Eiheiji-Cho, Yoshida-Gun, Fukui, 910-1193, Japan. miwano@u-fukui.ac.jp.

Classifications MeSH