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Congenital anomalies induced by triamcinolone acetonide in murine embryos
1Department of Pediatric Surgery, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Introduction:
We have studied the morphogenesis of anorectal malformations in mice using retinoids. Several investigators have reported an interaction between glucocorticoids and retinoids. It was supposed that glucocorticoids had some effects on the morphogenesis of murine embryos similar to retinoids. Therefore, we investigated alterations in the morphogenesis of murine embryos after triamcinolone acetonide (TAC) administration.
Material And Methods:
TAC was administered in a single dose (15 mg/kg or 30 mg/kg body weight) to pregnant ICR-SLC mice on embryonic day 7 (E7), 8, 9, and 10. They were sacrificed on E18, and fetuses were examined for internal and external malformations. Randomly chosen fetuses were embedded in paraffin for immunohistochemical staining of the glucocorticoid receptor (GR).
Results:
The groups given 15 mg/kg TAC had one peak in the incidence of cleft palate on E9 (100 %) and the groups given 30 mg/kg TAC showed a biphasic pattern in the incidence of cleft palate on E7 and E10. No other anomalies were found. GR expression was marked in the subepithelial layer of palatal processes in the treated specimens.
Conclusion:
The group given 15 mg/kg TAC on E9 provided a good model of cleft palate in ICR-SLC mice, and cleft palate was probably induced by various factors including disturbance of the bone morphogenetic protein (BMP) signaling pathway, shown by GR overexpression.
Insights
Triamcinolone acetonide (TAC) administration in mice can induce cleft palate, a birth defect. This study suggests glucocorticoid receptor overexpression may disrupt bone morphogenetic protein signaling, contributing to its development.
Area of Science:
- Developmental biology
- Teratology
- Pharmacology
Background:
- Retinoids are known to affect embryonic development.
- Glucocorticoids may share similar effects on murine embryo morphogenesis.
- Previous research suggests an interaction between glucocorticoids and retinoids.
Purpose of the Study:
- To investigate the effects of triamcinolone acetonide (TAC) on murine embryo morphogenesis.
- To determine if TAC can induce specific malformations, such as cleft palate.
- To explore the role of glucocorticoid receptor (GR) expression in TAC-induced defects.
Main Methods:
- Pregnant ICR-SLC mice were administered TAC (15 mg/kg or 30 mg/kg) on embryonic days 7-10.
- Fetuses were examined for external and internal malformations at embryonic day 18.
- Immunohistochemical staining was performed to assess glucocorticoid receptor (GR) expression in palatal tissues.
Main Results:
- TAC administration induced cleft palate in a dose- and time-dependent manner.
- A single dose of 15 mg/kg TAC on embryonic day 9 resulted in 100% cleft palate incidence.
- Glucocorticoid receptor (GR) expression was elevated in the palatal processes of TAC-treated fetuses.
Conclusions:
- Triamcinolone acetonide (TAC) administration on embryonic day 9 serves as a viable model for inducing cleft palate in mice.
- Cleft palate development is likely linked to disruptions in bone morphogenetic protein (BMP) signaling pathways.
- Overexpression of the glucocorticoid receptor (GR) may play a role in the teratogenic effects of TAC.
