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Podocyte-specific Translational Profiling In Vivo Uncovers Distinct Patterns in Trpc6-Deficient Podocytes
Jonas Einloft1, Andreas Hofmeister1, Mathieu Preußner1,2
1Department of Internal Medicine and Nephrology, University Hospital Giessen and Marburg, Philipps University Marburg, Marburg, Germany.
Summary
Canonical Transient Receptor Potential 6 (TRPC6) deficiency in podocytes causes distinct gene expression changes in young mice, but these effects diminish with age. This suggests TRPC6 plays a limited role in aging podocytes and kidney injury.
Area of Science:
- Nephrology
- Molecular Biology
- Genetics
Background:
- Canonical Transient Receptor Potential 6 (TRPC6) channels regulate podocyte function.
- While TRPC6 gain-of-function mutations cause kidney disease, the role of TRPC6 loss-of-function is less understood.
- TRPC6 deficiency does not cause overt kidney issues in mice, but mechanisms are unclear.
Purpose of the Study:
- To investigate the molecular and cellular basis of TRPC6-deficient podocytes.
- To analyze gene expression changes in TRPC6-deficient podocytes from young and aged mice.
Main Methods:
- Podocyte-specific Translational Ribosome Affinity Purification (TRAP) and RNA sequencing were used.
- Gene expression profiles of Trpc6-/- and wild-type mouse podocytes were compared at 9 and 78 weeks of age.
Main Results:
- Trpc6-/- mice showed no proteinuria or kidney abnormalities, even at old age.
- Young Trpc6-/- podocytes exhibited altered expression of genes involved in cytoskeleton, metabolism, and immune response.
- These transcriptional changes were significantly reduced in aged Trpc6-/- podocytes.
Conclusions:
- Young TRPC6-deficient podocytes display unique transcriptional signatures.
- These findings offer insights into TRPC6's role in podocyte protection or susceptibility to injury.
- The impact of TRPC6 deficiency is mild and diminishes with age, suggesting a reduced role in aging podocytes.
