Roles of glomerular endothelial hyaluronan in the development of proteinuria.


Journal

Physiological reports
ISSN: 2051-817X
Titre abrégé: Physiol Rep
Pays: United States
ID NLM: 101607800

Informations de publication

Date de publication:
09 2021
Historique:
revised: 01 08 2021
received: 01 08 2021
accepted: 04 08 2021
entrez: 2 9 2021
pubmed: 3 9 2021
medline: 25 2 2022
Statut: ppublish

Résumé

Vascular endothelial cells are covered with glycocalyx comprising heparan sulfate, hyaluronan, chondroitin sulfate, and associated proteins. Glomerular endothelial glycocalyx is involved in protecting against induction of proteinuria and structural damage, but the specific components in glycocalyx that represent therapeutic targets remain unclear. Anti-vascular endothelial growth factor (VEGF) therapy is associated with an increased risk of glomerular endothelial injury. This study investigated whether hyaluronan could provide a therapeutic target to protect against proteinuria. We conducted ex vivo and in vivo experiments to explore the effects of degrading glomerular hyaluronan by administering hyaluronidase and of supplementation with hyaluronan. We investigated hyaluronan expression using biotin-labeled hyaluronan-binding protein (HABP) in human kidney specimens or serum hyaluronan in endothelial injuries under inhibition of VEGF signaling. We directly demonstrated hyaluronan in glomerular endothelial layers using HABP staining. Ex vivo and in vivo experiments showed the development of proteinuria after digestion of hyaluronan in glomerular capillaries. Supplementation with hyaluronan after hyaluronidase treatment suppressed proteinuria. Mice in the in vivo study developed albuminuria after intraperitoneal injection of hyaluronidase with decreased glomerular hyaluronan and increased serum hyaluronan. In human kidneys with endothelial cell dysfunction and proteinuria due to inhibition of VEGF, glomerular expression of hyaluronan was reduced even in normal-appearing glomeruli. Serum hyaluronan levels were elevated in patients with pre-eclampsia with VEGF signaling inhibition. Our data suggest that hyaluronan itself plays crucial roles in preventing proteinuria and preserving the integrity of endothelial cells. Hyaluronan could provide a therapeutic target for preventing glomerular endothelial glycocalyx damage, including VEGF signaling inhibition.

Identifiants

pubmed: 34472715
doi: 10.14814/phy2.15019
pmc: PMC8411502
doi:

Substances chimiques

Hyaluronic Acid 9004-61-9
Hyaluronoglucosaminidase EC 3.2.1.35

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e15019

Informations de copyright

© 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.

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Auteurs

Akimasa Asai (A)

Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan.

Naoyuki Hatayama (N)

Department of Anatomy, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.

Keisuke Kamiya (K)

Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan.

Mai Yamauchi (M)

Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan.

Hiroshi Kinashi (H)

Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan.

Makoto Yamaguchi (M)

Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan.

Takayuki Katsuno (T)

Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan.

Hironobu Nobata (H)

Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan.

Kazushi Watanabe (K)

Department of Obstetrics and Gynecology, Aichi Medical University, Nagakute, Aichi, Japan.

Akihiko Wakatsuki (A)

Department of Obstetrics and Gynecology, Aichi Medical University, Nagakute, Aichi, Japan.

Jan Aten (J)

Department of Pathology, Amsterdam University Medical Center (Location AMC) University of Amsterdam, Amsterdam, The Netherlands.

Shoichi Maruyama (S)

Department of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.

Takuji Ishimoto (T)

Department of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.

Shuichi Hirai (S)

Department of Anatomy, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.

Munekazu Naito (M)

Department of Anatomy, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.

Yasuhiko Ito (Y)

Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute, Aichi, Japan.

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