Cyclin G1 and TASCC regulate kidney epithelial cell G2-M arrest and fibrotic maladaptive repair

Guillaume Canaud; Craig R. Brooks; Seiji Kishi; Kensei Taguchi; Kenji Nishimura; Sato Magassa; Adam Scott; Li-Li Hsiao; Takaharu Ichimura; Fabiola Terzi; Li Yang; Joseph V. Bonventre

doi:10.1126/scitranslmed.aav4754

Research ArticleKidney Fibrosis

Cyclin G1 and TASCC regulate kidney epithelial cell G₂-M arrest and fibrotic maladaptive repair

Guillaume Canaud¹,²,³,*,
View ORCID ProfileCraig R. Brooks ¹,⁴,*,
View ORCID ProfileSeiji Kishi¹,⁵,*,
View ORCID ProfileKensei Taguchi⁴,
Kenji Nishimura⁵,
Sato Magassa²,
View ORCID ProfileAdam Scott¹,⁶,
View ORCID ProfileLi-Li Hsiao¹,
View ORCID ProfileTakaharu Ichimura¹,
Fabiola Terzi²,
Li Yang⁷ and
View ORCID ProfileJoseph V. Bonventre ¹,⁸,⁹,†

¹Renal Division, Brigham and Women’s Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.
²INSERM U1151, Institut Necker-Enfants Malades, Université Paris Descartes, Paris 75743, France.
³Service de Néphrologie et Transplantation Adultes, Hôpital Necker-Enfants Malades, Paris 75743, France.
⁴Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
⁵Department of Nephrology, Graduate School of Biomedical Sciences, Tokushima University, Tokushima 7708503, Japan.
⁶Division of Nephrology, Department of Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
⁷Renal Division, Peking University First Hospital, Beijing 100871, China.
⁸Division of Health Sciences and Technology, Harvard–Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
⁹Harvard Stem Cell Institute, Cambridge, MA 02138, USA.

↵†Corresponding author. Email: joseph_bonventre{at}hms.harvard.edu

↵* These authors contributed equally to this work as co-first authors.

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Science Translational Medicine 23 Jan 2019:
Vol. 11, Issue 476, eaav4754
DOI: 10.1126/scitranslmed.aav4754

Guillaume Canaud

1Renal Division, Brigham and Women’s Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.

2INSERM U1151, Institut Necker-Enfants Malades, Université Paris Descartes, Paris 75743, France.

3Service de Néphrologie et Transplantation Adultes, Hôpital Necker-Enfants Malades, Paris 75743, France.

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Craig R. Brooks

1Renal Division, Brigham and Women’s Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.

4Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.

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Seiji Kishi

1Renal Division, Brigham and Women’s Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.

5Department of Nephrology, Graduate School of Biomedical Sciences, Tokushima University, Tokushima 7708503, Japan.

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Kensei Taguchi

4Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.

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Kenji Nishimura

5Department of Nephrology, Graduate School of Biomedical Sciences, Tokushima University, Tokushima 7708503, Japan.

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Sato Magassa

2INSERM U1151, Institut Necker-Enfants Malades, Université Paris Descartes, Paris 75743, France.

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Adam Scott

1Renal Division, Brigham and Women’s Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.

6Division of Nephrology, Department of Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.

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Li-Li Hsiao

1Renal Division, Brigham and Women’s Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.

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Takaharu Ichimura

1Renal Division, Brigham and Women’s Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.

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Fabiola Terzi

2INSERM U1151, Institut Necker-Enfants Malades, Université Paris Descartes, Paris 75743, France.

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Li Yang

7Renal Division, Peking University First Hospital, Beijing 100871, China.

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Joseph V. Bonventre

1Renal Division, Brigham and Women’s Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.

8Division of Health Sciences and Technology, Harvard–Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

9Harvard Stem Cell Institute, Cambridge, MA 02138, USA.

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For correspondence: joseph_bonventre@hms.harvard.edu

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Taking kidney fibrosis to TASCC

The kidney has an inherent capacity to recover from acute injury; however, severe injury can lead to chronic kidney disease and fibrosis. Canaud et al. studied kidney epithelial cells’ maladaptive response to injury. The formation of target of rapamycin–autophagy spatial coupling compartments (TASCCs) in proximal epithelial cells was associated with cell cycle arrest and fibrosis in human chronic kidney disease, whereas knocking out cyclin G1 prevented TASCC formation and fibrosis in mouse models. This study provides mechanistic insight into renal fibrosis and identifies a potential therapeutic target.

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Cyclin G1 and TASCC regulate kidney epithelial cell G₂-M arrest and fibrotic maladaptive repair

Taking kidney fibrosis to TASCC

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Cyclin G1 and TASCC regulate kidney epithelial cell G₂-M arrest and fibrotic maladaptive repair

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