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Related Experiment Videos

Angiotensin type II receptor expression and ureteral budding.

K Oshima1, Y Miyazaki, J W Brock

  • 1Department of Pediatric Urology, Vanderbilt Children's Hospital, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

The Journal of Urology
|October 5, 2001
PubMed
Summary
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Methods in molecular medicine·2011

Deletion of the angiotensin type II receptor gene (Agtr2) in mice causes urinary tract anomalies. Agtr2 expression may inhibit abnormal ureteral budding, preventing congenital kidney and urinary tract defects.

Area of Science:

  • Developmental Biology
  • Genetics
  • Urology

Background:

  • Congenital anomalies of the kidney and urinary tract (CAKUT) affect 1 in 500 live births.
  • Mouse models with angiotensin type II receptor (Agtr2) gene deletion exhibit urinary tract abnormalities mirroring human conditions.
  • The precise mechanism underlying Agtr2-associated urinary tract malformations remains unclear.

Purpose of the Study:

  • To investigate the role of angiotensin type II receptor (Agtr2) expression in normal and aberrant ureteral budding during embryonic development.
  • To elucidate the mechanism by which Agtr2 influences urinary tract formation.

Main Methods:

  • Comparative analysis of wild-type and Agtr2-null mouse embryos and newborns.
  • In situ hybridization techniques to detect Agtr2 expression and c-ret (a marker for ureteral budding).

Related Experiment Videos

  • Gross morphological examination and histological analysis of urinary tracts at various embryonic and neonatal stages.

    • Main Results:

    • Agtr2 knockout newborns showed a 3.1% incidence of urinary tract abnormalities, primarily duplicated collecting systems.
    • Nearly 60% of Agtr2 knockout embryos displayed abnormal ureteral budding.
    • Agtr2 expression was detected in wild-type embryos at the ectopic ureteral budding site.

    Conclusions:

    • Angiotensin type II receptor (Agtr2) plays a role in inhibiting aberrant ureteral budding during urinary tract development.
    • Defects in Agtr2 function can lead to ectopic ureteral budding, potentially causing CAKUT.
    • Agtr2 is a significant, though not exclusive, regulator of normal urinary tract embryogenesis.