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Effect of glomerular disease on the podocyte cell cycle

ABSTRACT: Proteomic data from three populations of sorted murine podocytes using the FUCCI (fluorescence ubiquitination cell cycle indicator) Cell Cycle Sensor: Wild-Type podocytes at G0 (WT_G0), Alport Syndrome podocytes at G0 (AS_G0), and Alport Syndrome podocytes at G1 (AS_G1). Cell populations were sorted from murine kidney; ~10K cells were prepared using the MicroPOTS protocol (PMID: 30460388), digested with trypsin, then analyzed by LC-MS/MS. Data was searched with MaxQuant.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Geremy Clair

PROVIDER: MSV000086705 | MassIVE | Fri Jan 15 10:48:00 GMT 2021

SECONDARY ACCESSION(S): PXD023632

REPOSITORIES: MassIVE

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Effect of disease progression on the podocyte cell cycle in Alport Syndrome.

Frank Camille Nicolas CN Hou Xiaogang X Petrosyan Astgik A Villani Valentina V Zhao Rui R Hansen Joshua R JR Clair Geremy G Salem Fadi F De Filippo Roger E RE Cravedi Paolo P Lemley Kevin V KV Perin Laura L

Kidney international 20210923 1

Progression of glomerulosclerosis is associated with loss of podocytes with subsequent glomerular tuft instability. It is thought that a diminished number of podocytes may be able to preserve tuft stability through cell hypertrophy associated with cell cycle reentry. At the same time, reentry into the cell cycle risks podocyte detachment if podocytes cross the G1/S checkpoint and undergo abortive cytokinesis. In order to study cell cycle dynamics during chronic kidney disease (CKD) development, ...[more]

PMID: 34562503

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