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Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli
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Podocyte injury in diabetic nephropathy: implications of angiotensin II-dependent activation of TRPC channels

Daria V Ilatovskaya1, Vladislav Levchenko1, Andrea Lowing1

  • 1Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.

Scientific Reports
|December 15, 2015
PubMed

Insights

Diabetic kidney disease involves podocyte injury due to abnormal calcium handling. Angiotensin II (Ang II) exacerbates this in type 1 diabetic nephropathy by activating Transient Receptor Potential Canonical (TRPC) channels in podocytes.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Physiology

Background:

  • Podocyte injury is a key factor in diabetic kidney disease (DN), leading to proteinuria and glomerulosclerosis.
  • Dysfunctional calcium handling, particularly via Transient Receptor Potential Canonical (TRPC) channels, contributes to podocyte loss.
  • Elevated Angiotensin II (Ang II) levels in diabetes activate TRPC6 channels in podocytes.

Purpose of the Study:

  • To investigate if Angiotensin II-mediated calcium influx is heightened in podocytes during type 1 diabetic nephropathy.
  • To explore the role of TRPC channels in Ang II-induced calcium handling abnormalities in diabetic podocytes.

Main Methods:

  • Induction of type 1 diabetes in Dahl Salt-Sensitive rats using streptozotocin (STZ-SS).
  • Assessment of diabetic nephropathy markers (hyperglycemia, albuminuria, etc.) after 11 weeks.
  • Patch-clamp electrophysiology on freshly isolated glomeruli podocytes to measure TRPC channel activity and calcium influx.

Main Results:

  • STZ-SS rats exhibited hallmark signs of diabetic nephropathy.
  • Podocytes from STZ-SS rats showed increased basal TRPC channel activity.
  • Ang II application resulted in a greater calcium influx in podocytes from diabetic rats compared to controls.

Conclusions:

  • Angiotensin II-mediated calcium influx is indeed aggravated in podocytes under type 1 diabetic nephropathy conditions.
  • Enhanced TRPC channel activity plays a significant role in the calcium dysregulation observed in diabetic podocytes.
  • These findings advance the understanding of TRPC channel involvement in podocytopenia during diabetic kidney disease initiation.

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