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Polycystic kidney disease in SBM transgenic mice: role of c-myc in disease induction and progression.

Publication ,  Journal Article
Trudel, M; Barisoni, L; Lanoix, J; D'Agati, V
Published in: The American journal of pathology
January 1998

SBM mouse is a unique transgenic model of polycystic kidney disease (PKD) produced by dysregulation of c-myc in the kidneys. Our previous demonstration that c-myc is overexpressed in human autosomal polycystic kidney disease (ADPKD) prompted us to investigate the pathogenetic role of c-myc in the induction and progression of the cystogenic phenotype in our mouse model. In young SBM kidneys, c-myc was two- to threefold increased with persistent expression levels into adulthood, an age when c-myc is normally undetectable. In situ hybridization analysis of the c-myc transgene demonstrated intense signal specifically overlying glomerular and tubular epithelium of developing cysts in fetal and young kidneys. Increased expression of c-myc correlated with the initiation and progression of the PKD phenotype as evidenced by early tubular and glomerular cysts at E16.5. Cyst number and size increased with age, with co-development of glomerular and tubular epithelial hyperplasia. Consistently, the mean renal proliferative index was increased approximately 5- to 20-fold in noncystic and cystic tubules of newborn SBM animals compared with littermate controls. Similarly, in fetal and newborn kidneys the tubular apoptotic indices were increased approximately three- to ninefold over controls. Both proliferation and apoptotic rates in cystic tubules approached levels in developing tubules from the normal nephrogenic zone. We conclude that the pathogenesis of PKD hinges on a critical imbalance in c-myc regulation of the opposing processes of cell proliferation and apoptosis, recapitulating the cellular phenomena in developing fetal kidney.

Duke Scholars

Published In

The American journal of pathology

EISSN

1525-2191

ISSN

0002-9440

Publication Date

January 1998

Volume

152

Issue

1

Start / End Page

219 / 229

Related Subject Headings

  • Transcription, Genetic
  • Proto-Oncogene Proteins c-myc
  • Polymerase Chain Reaction
  • Polycystic Kidney Diseases
  • Pathology
  • Mice, Transgenic
  • Mice
  • Kidney
  • In Situ Hybridization
  • Fetus
 

Citation

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Chicago
ICMJE
MLA
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Trudel, M., Barisoni, L., Lanoix, J., & D’Agati, V. (1998). Polycystic kidney disease in SBM transgenic mice: role of c-myc in disease induction and progression. The American Journal of Pathology, 152(1), 219–229.
Trudel, M., L. Barisoni, J. Lanoix, and V. D’Agati. “Polycystic kidney disease in SBM transgenic mice: role of c-myc in disease induction and progression.The American Journal of Pathology 152, no. 1 (January 1998): 219–29.
Trudel M, Barisoni L, Lanoix J, D’Agati V. Polycystic kidney disease in SBM transgenic mice: role of c-myc in disease induction and progression. The American journal of pathology. 1998 Jan;152(1):219–29.
Trudel, M., et al. “Polycystic kidney disease in SBM transgenic mice: role of c-myc in disease induction and progression.The American Journal of Pathology, vol. 152, no. 1, Jan. 1998, pp. 219–29.
Trudel M, Barisoni L, Lanoix J, D’Agati V. Polycystic kidney disease in SBM transgenic mice: role of c-myc in disease induction and progression. The American journal of pathology. 1998 Jan;152(1):219–229.
Journal cover image

Published In

The American journal of pathology

EISSN

1525-2191

ISSN

0002-9440

Publication Date

January 1998

Volume

152

Issue

1

Start / End Page

219 / 229

Related Subject Headings

  • Transcription, Genetic
  • Proto-Oncogene Proteins c-myc
  • Polymerase Chain Reaction
  • Polycystic Kidney Diseases
  • Pathology
  • Mice, Transgenic
  • Mice
  • Kidney
  • In Situ Hybridization
  • Fetus