Protein tyrosine phosphatase 1B deficiency in podocytes mitigates hyperglycemia-induced renal injury.

ABSTRACT:

Objective

Diabetic nephropathy is one of the most devastating complications of diabetes, and growing evidence implicates podocyte dysfunction in disease pathogenesis. The objective of this study was to investigate the contribution of protein tyrosine phosphatase 1B (PTP1B) in podocytes to hyperglycemia-induced renal injury.

Methods

To determine the in vivo function of PTP1B in podocytes we generated mice with podocyte-specific PTP1B disruption (hereafter termed pod-PTP1B KO). Kidney functions were determined in control and pod-PTP1B KO mice under normoglycemia and high-fat diet (HFD)- and streptozotocin (STZ)-induced hyperglycemia.

Results

PTP1B expression increased in murine kidneys following HFD and STZ challenges. Under normoglycemia control and pod-PTP1B KO mice e

SUBMITTER: Ito Y 

PROVIDER: S-EPMC5690491 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature