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Updated: Apr 16, 2026

Fetal Echocardiography and Pulsed-wave Doppler Ultrasound in a Rabbit Model of Intrauterine Growth Restriction
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Published on: June 29, 2013

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Dynamic p53 protein expression and phosphorylation in the kidneys of rats that experienced intrauterine growth

Xiaori He1, Zongde Xie, Qingyi Dong

  • 1a Department of Neonatology, Second Xiangya Hospital , Central South University , Changsha , Hunan , PR China.

Renal Failure
|February 28, 2015
PubMed
Abstract

Insights

Maternal malnutrition causes intrauterine growth restriction (IUGR), impacting kidney development. This study reveals that IUGR in pups is linked to increased p53-p21 signaling in the kidney.

Area of Science:

  • Nephrology
  • Developmental Biology
  • Molecular Biology

Background:

  • Intrauterine growth restriction (IUGR) is a significant concern affecting fetal development and long-term health.
  • Understanding the molecular mechanisms underlying IUGR is crucial for developing effective interventions.

Purpose of the Study:

  • To investigate the molecular mechanisms involved in intrauterine growth restriction (IUGR) in a rat model.
  • To examine the role of p53 signaling pathways in the kidney during IUGR.

Main Methods:

  • An intrauterine growth restriction (IUGR) model was established in Sprague-Dawley rats using a low-protein diet.
  • Protein expression, phosphorylation, and apoptosis were assessed using Western blot, immunohistochemistry, and TUNEL staining.
  • MDM2 mRNA expression was quantified via real-time PCR.

Main Results:

  • IUGR pups exhibited significantly lower body and kidney weights, and reduced glomerular numbers compared to controls.
  • Kidney tissues from IUGR pups showed significantly higher p53 protein levels and p53 phosphorylation at Ser(15) compared to controls.
  • Increased p21 expression and significant apoptosis were observed in the kidneys of IUGR pups.

Conclusions:

  • Malnutrition-induced IUGR is associated with the activation of the p53-p21 signaling pathway in the kidney.
  • This activation may contribute to kidney developmental abnormalities observed in IUGR.
  • Further research is warranted to explore therapeutic strategies targeting this pathway.
Keywords:
Glomerular numberintrauterine growth restrictionkidneyp53phosphorylation

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