PUBLICATION

Circulating factors cause proteinuria in parabiotic zebrafish

Authors
Müller-Deile, J., Schenk, H., Schroder, P., Schulze, K., Bolaños-Palmieri, P., Siegerist, F., Endlich, N., Haller, H., Schiffer, M.
ID
ZDB-PUB-190512-2
Date
2019
Source
Kidney International   96(2): 342-349 (Journal)
Registered Authors
Keywords
nephrotic syndrome, podocyte, proteinuria
MeSH Terms
  • Animals
  • Embryo, Nonmammalian
  • Extracellular Matrix Proteins/genetics*
  • Gene Expression Regulation
  • Gene Knockdown Techniques
  • Glomerulosclerosis, Focal Segmental/blood*
  • Glomerulosclerosis, Focal Segmental/genetics
  • Glomerulosclerosis, Focal Segmental/pathology
  • Humans
  • Microscopy, Electron, Transmission
  • Morpholinos/genetics
  • Parabiosis
  • Podocytes/pathology*
  • Podocytes/ultrastructure
  • Proteinuria/blood*
  • Proteinuria/genetics
  • Proteinuria/pathology
  • Zebrafish
  • Zebrafish Proteins/blood
  • Zebrafish Proteins/genetics*
PubMed
31076096 Full text @ Kidney Int.
Abstract
Proteinuria can be induced by impairment of any component of the glomerular filtration barrier. To determine the role of circulating permeability factors on glomerular damage, we developed a parabiosis-based zebrafish model to generate a common circulation between zebrafish larvae. A morpholino-mediated knockdown of a podocyte specific gene (nephronectin) was induced in one zebrafish larva which was then fused to an un-manipulated fish. Notably, proteinuria and glomerular damage were present in the manipulated fish and in the parabiotically-fused partner. Thus, circulating permeability factors may be induced by proteinuria even when an induced podocyte gene dysregulation is the initiating cause.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping