Enhanced podocyte vesicle transport in the nephrotic rat
Akihiro Tojo1, Saaya Hatakeyama2, Satoshi Kinugasa2
1Division of Nephrology and Endocrinology, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan. akitojo-tky@umin.ac.jp.
Medical Molecular Morphology
|March 19, 2017
Summary
Podocyte endocytosis of albumin increases in minimal change nephrotic syndrome. This study reveals enhanced vesicle transport and elevated cytoplasmic dynein and myosin proteins in affected rat podocytes.
Area of Science:
- Nephrology
- Cell Biology
- Molecular Biology
Background:
- Minimal change nephrotic syndrome (MCNS) is characterized by increased albuminuria.
- Podocyte injury is central to MCNS pathogenesis, with enhanced albumin endocytosis observed.
Purpose of the Study:
- To investigate the mechanism of endocytic vesicle transport in podocytes during puromycin aminonucleoside (PAN)-induced nephrotic syndrome.
- To identify proteins involved in altered vesicle transport in MCNS.
Main Methods:
- Induction of nephrotic syndrome in rats using PAN.
- Intravenous injection of Evans Blue-labeled albumin followed by kidney fixation for morphological analysis.
- Isolation of glomeruli for protein analysis via gel electrophoresis and mass spectrometry.
Main Results:
- Evans Blue-labeled albumin accumulated in an increased number of vesicles within podocytes of PAN-induced nephrotic rats.
- Three-dimensional observation indicated vesicle transport from the cytoplasm to the podocyte apical membrane.
- Mass spectrometry identified increased levels of cytoplasmic dynein 1 heavy chain, myosin IX, and myosin VIIb in nephrotic rat glomeruli.
Conclusions:
- Podocyte endocytic vesicle accumulation carrying albumin is significantly increased in experimental MCNS.
- Elevated levels of cytoplasmic dynein and myosin are associated with enhanced albumin transport in podocytes during MCNS.
- These findings elucidate a potential mechanism for albumin handling in podocytes during nephrotic syndrome.
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