# Morphological Alterations of Conal Ridges and Differential Expression of AP2α in the Offspring Hearts of Experimental Diabetic Rats

**Authors:** Tania Cristina Ramírez-Fuentes, Ricardo Jaime-Cruz, Carlos César Patiño-Morales, Laura Villavicencio-Guzmán, Juan Carlos Corona, María Cristina Revilla-Monsalve, Rosa Adriana Jarillo-Luna, Marcela Salazar-García

PMC · DOI: 10.3390/ijms26115061 · 2025-05-24

## TL;DR

This study shows that a high-glucose environment during pregnancy causes heart defects in rat offspring by altering conal ridge development and AP2α expression.

## Contribution

The study identifies AP2α expression changes and conal ridge morphological alterations as novel indicators of heart defects caused by maternal hyperglycemia.

## Key findings

- Hearts of offspring in the experimental group showed smaller dimensions compared to controls at 13, 15, and 17 DPC.
- Hyperglycemia altered AP2α immunostaining in offspring hearts at all three developmental stages.
- Conotruncal heart defects, including double outlet of the right ventricle and AV canal, were prominent in hyperglycemic offspring.

## Abstract

Neural crest cells (NCCs) play a significant role in the development of ventricular outflow tracts (OFTs), and cardiac neural crest cells (cNCCs) are involved in the development of the embryonic conus, suggesting that these cell lineages may be a teratogenic target for the development of cardiopathies in offspring conceived under a hyperglycemic environment. We evaluate the effect of the hyperglycemic intrauterine environment on the morphological and anatomical changes in the conal ridges along with the alterations in the spatiotemporal expression of AP2α in offspring hearts at 13, 15, and 17 DPC. The anatomical and histological analysis of the hearts in the experimental group presented smaller dimensions compared to the control group in the offspring at the three ages studied. Consequently, this resulted in a hyperglycemic environment that altered the immunostaining of AP2α in the hearts of the offspring at the three ages studied. Thus, the hyperglycemic intrauterine environment in offspring caused important morphological alterations in the development of conal ridges and promoted the generation of conotruncal heart defects in which the double outlet of the right ventricle, the atrioventricular (AV) canal, predominated. Therefore, knowing that exposing the offspring to more glucose potentially can lead to complications during organogenesis of the circulatory and central nervous systems.

## Linked entities

- **Genes:** AP2a (APETALA2a) [NCBI Gene 100191138]
- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** Fabp4 (fatty acid binding protein 4) [NCBI Gene 79451] {aka Albp, aP2}
- **Diseases:** Diabetic (MESH:D003920), hyperglycemic (MESH:D006944), conotruncal heart defects (MESH:C535464), cardiopathies (MESH:C536187)
- **Chemicals:** glucose (MESH:D005947)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12155284/full.md

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Source: https://tomesphere.com/paper/PMC12155284