The integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulus

Abstract The kidney glomerulus is a filtration barrier in which capillary loop architecture depends on epithelial-stromal interactions between podocytes and mesangial cells. Podocytes are terminally differentiated cells within the glomerulus that express YAP and TAZ. Here we test the hypotheses that...

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Main Authors: Evelyne Huynh-Cong, Victoria Driscoll, Sandrine Ettou, Keith Keller, Amha Atakilit, Mary E. Taglienti, Saurabh Kumar, Astrid Weins, Valerie A. Schumacher, Jordan A. Kreidberg
Format: Article
Language:English
Published: Nature Portfolio 2025-04-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-58567-y
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author Evelyne Huynh-Cong
Victoria Driscoll
Sandrine Ettou
Keith Keller
Amha Atakilit
Mary E. Taglienti
Saurabh Kumar
Astrid Weins
Valerie A. Schumacher
Jordan A. Kreidberg
author_facet Evelyne Huynh-Cong
Victoria Driscoll
Sandrine Ettou
Keith Keller
Amha Atakilit
Mary E. Taglienti
Saurabh Kumar
Astrid Weins
Valerie A. Schumacher
Jordan A. Kreidberg
author_sort Evelyne Huynh-Cong
collection DOAJ
description Abstract The kidney glomerulus is a filtration barrier in which capillary loop architecture depends on epithelial-stromal interactions between podocytes and mesangial cells. Podocytes are terminally differentiated cells within the glomerulus that express YAP and TAZ. Here we test the hypotheses that YAP and TAZ are required in podocytes to maintain capillary loop architecture and that shifts in the integrin repertoire during podocyte injury affect transcriptional activity of YAP and TAZ. Loss of YAP in podocytes of adult mice renders them more sensitive to injury, whereas loss of both YAP and TAZ in podocytes rapidly compromises the filtration barrier. α3β1 and αvβ5 are two prominent integrins on murine podocytes. Podocyte injury or loss of α3β1 leads to increased abundance of αvβ5 and nuclear localization of YAP. In vitro, blockade of αvβ5 decreases nuclear YAP. Increased αv integrins are found in human kidney disease. Thus, our studies demonstrate the crucial regulatory interplay between cell adhesion and transcriptional regulation as an important determinant of human disease.
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spelling doaj-art-92b32e74f7ca48b19db1e8a1921bd4a02025-08-20T02:17:10ZengNature PortfolioNature Communications2041-17232025-04-0116111710.1038/s41467-025-58567-yThe integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulusEvelyne Huynh-Cong0Victoria Driscoll1Sandrine Ettou2Keith Keller3Amha Atakilit4Mary E. Taglienti5Saurabh Kumar6Astrid Weins7Valerie A. Schumacher8Jordan A. Kreidberg9Department of Urology, Boston Children’s HospitalDivision of Nephrology, Beth Israel Deaconess Medical CenterDepartment of Urology, Boston Children’s HospitalDepartment of Pathology, Brigham and Women’s Hospital and Harvard Medical SchoolLung Biology Center, Department of Medicine, University of California San FranciscoDepartment of Urology, Boston Children’s HospitalDepartment of Urology, Boston Children’s HospitalDepartment of Pathology, Brigham and Women’s Hospital and Harvard Medical SchoolDepartment of Urology, Boston Children’s HospitalDepartment of Urology, Boston Children’s HospitalAbstract The kidney glomerulus is a filtration barrier in which capillary loop architecture depends on epithelial-stromal interactions between podocytes and mesangial cells. Podocytes are terminally differentiated cells within the glomerulus that express YAP and TAZ. Here we test the hypotheses that YAP and TAZ are required in podocytes to maintain capillary loop architecture and that shifts in the integrin repertoire during podocyte injury affect transcriptional activity of YAP and TAZ. Loss of YAP in podocytes of adult mice renders them more sensitive to injury, whereas loss of both YAP and TAZ in podocytes rapidly compromises the filtration barrier. α3β1 and αvβ5 are two prominent integrins on murine podocytes. Podocyte injury or loss of α3β1 leads to increased abundance of αvβ5 and nuclear localization of YAP. In vitro, blockade of αvβ5 decreases nuclear YAP. Increased αv integrins are found in human kidney disease. Thus, our studies demonstrate the crucial regulatory interplay between cell adhesion and transcriptional regulation as an important determinant of human disease.https://doi.org/10.1038/s41467-025-58567-y
spellingShingle Evelyne Huynh-Cong
Victoria Driscoll
Sandrine Ettou
Keith Keller
Amha Atakilit
Mary E. Taglienti
Saurabh Kumar
Astrid Weins
Valerie A. Schumacher
Jordan A. Kreidberg
The integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulus
Nature Communications
title The integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulus
title_full The integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulus
title_fullStr The integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulus
title_full_unstemmed The integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulus
title_short The integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulus
title_sort integrin repertoire drives yap dependent epithelial stromal interactions during injury of the kidney glomerulus
url https://doi.org/10.1038/s41467-025-58567-y
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