Podocyte expression of nonmuscle myosin heavy chain-IIA decreases in idiopathic nephrotic syndrome, especially in focal segmental glomerulosclerosis

Nephrol Dial Transplant. 2013 Dec;28(12):2993-3003. doi: 10.1093/ndt/gft350. Epub 2013 Sep 15.

Abstract

Background: Previous studies have identified significant associations between the development of idiopathic focal segmental glomerulosclerosis (FSGS) and MYH9 encoding nonmuscle myosin heavy chain-IIA (NMMHC-IIA). However, these studies focused only on the linkage of MYH9 polymorphisms and development of FSGS. There have been no reports on pathological changes of NMMHC-IIA in human glomerular diseases. Here we report on the precise localization of NMMHC-IIA in podocytes and changes in NMMHC-IIA expression in pathological states in rats and humans.

Methods: Immunocytochemical (immunofluorescence and immunoelectron microscopy) studies were performed to determine the precise localization of NMMHC-IIA. Expression levels of NMMHC-IIA were investigated in puromycin aminonucleoside (PAN)-treated rats; and expression levels of NMMHC-IIA and other podocyte-related proteins were investigated in glomeruli of patients with idiopathic FSGS and other heavy proteinuric glomerular diseases.

Results: NMMHC-IIA was located primarily at the cell body and primary processes of podocytes; this localization is distinct from other podocyte-related molecules causing hereditary FSGS. In PAN-treated rat kidneys, expression levels of NMMHC-IIA in podocytes decreased. Immunohistochemical analysis revealed that expression levels of NMMHC-IIA markedly decreased in idiopathic nephrotic syndrome, especially FSGS, whereas it did not change in other chronic glomerulonephritis showing apparent proteinuria. Changes in NMMHC-IIA expression were observed in glomeruli where expression of nephrin and synaptopodin was maintained.

Conclusions: Considering previous genome-wide association studies and development of FSGS in patients with MYH9 mutations, the characteristic localization of NMMHC-IIA and the specific decrease in NMMHC-IIA expression in idiopathic nephrotic syndrome, especially FSGS, suggest the important role of NMMHC-IIA in the development of FSGS.

Keywords: focal segmental glomerulosclerosis; myh9; nonmuscle myosin heavy chain-IIA; podocyte; primary process.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Animals
  • Biomarkers / analysis
  • Child
  • Child, Preschool
  • Chronic Disease
  • Female
  • Glomerulonephritis / metabolism*
  • Glomerulonephritis / pathology
  • Glomerulosclerosis, Focal Segmental / metabolism*
  • Glomerulosclerosis, Focal Segmental / pathology
  • Humans
  • Kidney Glomerulus / metabolism*
  • Kidney Glomerulus / pathology
  • Male
  • Microscopy, Electron
  • Middle Aged
  • Molecular Motor Proteins / metabolism*
  • Myosin Heavy Chains / metabolism*
  • Podocytes / metabolism*
  • Podocytes / pathology
  • Proteinuria / metabolism*
  • Proteinuria / pathology
  • Rats
  • Rats, Wistar

Substances

  • Biomarkers
  • MYH9 protein, human
  • Molecular Motor Proteins
  • Myosin Heavy Chains