Glucocorticoid inhibition of RNA synthesis and the critical period for cleft palate induction in inbred mice

Andrew, F. D.; Bowen, Donna; Zimmerman, Ernest F.

doi:10.1002/tera.1420070208

Cited by 36 publications

(4 citation statements)

References 20 publications

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“…Glucocorticoids inhibit RNA synthesis in the palatal shelves [5] or induce the formation of small palatal shelves due to a decrease in mitotic density [4,9,12]. Kurisu et al observed TAC induced retardation of the elevation of palatal shelves, and degradation of MEE cells within a half or one day [13].…”

Section: Discussionmentioning

confidence: 99%

Histopathological Findings of Cleft Palate in Rat Embryos Induced by Triamcinolone Acetonide

Furukawa

Usuda

Abe

et al. 2004

The Journal of Veterinary Medical Science

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ABSTRACT. Triamcinolone acetonide (TAC), a synthetic glucocorticoid, induces cleft palate resulting from poor development of palatal shelves in mice. However, TAC has no effect on medial edge epithelial cells (MEE cells) in secondary palatal shelves. In the present study, we examined the relationship between the pathogenesis of cleft palate and the effects on MEE cells and palatal mesenchyma l cells in rat embryos/fetuses exposed to TAC. Pregnant Wistar Hannover rats were given TAC intramuscularly at 0.5 mg/kg at gestation d ays (Day) 12, 13, and 14, then embryos/fetuses were harvested on Days 14.5, 15, 16 and 20. The effects of TAC were as follows; an inhibition of palatal mesenchymal cell proliferation on Day 14.5, a decrease in the density of palatal mesenchymal cells and MEE cells, and expression of epidermal growth factor (EGF) receptors in MEE cells on Day 15, and stratified squamous differentiation of MEE cel ls with expression of cytokeratin and EGF receptors on Day 16. These findings indicated that TAC inhibited the proliferation of mesenchymal cells and affected the differentiation of MEE cells into stratified squamous epithelia in the palatal shelves of rat embryos. H owever, these stratified squamous MEE cells partially fused with each other. Thus, we suspected that a major contributing factor to the formation of TAC-induced cleft palate might not be the altered differentiation of MEE cells, but the inhibition of mesenchymal cell proliferation. KEY WORDS: cleft palate, MEE cell, rat, triamcinolone acetonide, Wistar Hannover.

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Section: Discussionmentioning

confidence: 99%

Histopathological Findings of Cleft Palate in Rat Embryos Induced by Triamcinolone Acetonide

Furukawa

Usuda

Abe

et al. 2004

The Journal of Veterinary Medical Science

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“…Although cleft palates could be induced by triamcinolone in murine C3H strains when administered at E11.5 (Andrew et al 1973), the C3H background probably is not sufficiently modeling human cleft palates (Juriloff and Harris 2008). …”

Section: Discussionmentioning

confidence: 99%

Viable Ednra Y129F mice feature human mandibulofacial dysostosis with alopecia (MFDA) syndrome due to the homologue mutation

et al. 2016

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Animal models resembling human mutations are valuable tools to research the features of complex human craniofacial syndromes. This is the first report on a viable dominant mouse model carrying a non-synonymous sequence variation within the endothelin receptor type A gene (Ednra c.386A>T, p.Tyr129Phe) derived by an ENU mutagenesis program. The identical amino acid substitution was reported recently as disease causing in three individuals with the mandibulofacial dysostosis with alopecia (MFDA, OMIM 616367) syndrome. We performed standardized phenotyping of wild-type, heterozygous, and homozygous Ednra Y129F mice within the German Mouse Clinic. Mutant mice mimic the craniofacial phenotypes of jaw dysplasia, micrognathia, dysplastic temporomandibular joints, auricular dysmorphism, and missing of the squamosal zygomatic process as described for MFDA-affected individuals. As observed in MFDA-affected individuals, mutant Ednra Y129F mice exhibit hearing impairment in line with strong abnormalities of the ossicles and further, reduction of some lung volumetric parameters. In general, heterozygous and homozygous mice demonstrated inter-individual diversity of expression of the craniofacial phenotypes as observed in MFDA patients but without showing any cleft palates, eyelid defects, or alopecia. Mutant Ednra Y129F mice represent a valuable viable model for complex human syndromes of the first and second pharyngeal arches and for further studies and analysis of impaired endothelin 1 (EDN1)–endothelin receptor type A (EDNRA) signaling. Above all, Ednra Y129F mice model the recently published human MFDA syndrome and may be helpful for further disease understanding and development of therapeutic interventions.Electronic supplementary materialThe online version of this article (doi:10.1007/s00335-016-9664-5) contains supplementary material, which is available to authorized users.

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“…On day 14 of gestation animals were killed by cervical dislocation and gravid uteri were placed on ice. This is approximately 24 h prior to in situ shelf reorientation (Andrew, Bowen & Zimmerman, 1973). Embryos were removed and examined; those with cleft lip were eliminated.…”

Section: Animals and Culture Systemmentioning

confidence: 99%

The effect of reducing ATP levels on reorientation of the secondary palate

Bulleit

Zimmerman²

1986

Development

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The force for directing palate shelf reorientation appears to be associated with elements of the presumptive hard palate (Brinkley & Vickerman, 1979; Bulleit & Zimmerman, 1985). The palatal elements that mediate this process do not require palate cells to be metabolically active for expression of the force. This contention was demonstrated using an in vitro system that allows substantial reorientation of the hard palate to occur. ATP levels were reduced by treatment with metabolic inhibitors and the degree of reorientation was measured 1 h following pretreatment with inhibitors. Treatment of cultured embryonic heads under anoxic conditions with 2,4-dinitrophenol or KCN had noeffect on the degree of reorientation occurring in vitro. These agents reduced ATP levels by 71 % and 62 %, respectively. Treatment of cultured heads with 2-deoxy-D-glucose under anoxia also had no effect on reorientation. This treatment reduced ATP levels in embryonic heads by 92–94%. A similar reduction was observed if ATP levels were measured in palate tissue alone. The treatment of cultured heads with 2-deoxy-D-glucose and anoxia not only reduced levels of ATP but also reduced CTP, GTP and UTP. These results indicate that palate shelf reorientation is independent of cellular metabolic activity and supports the hypothesis that reorientation is dependent on a pre-existing infrastructure within the palate shelves.

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Glucocorticoid inhibition of RNA synthesis and the critical period for cleft palate induction in inbred mice

Cited by 36 publications

References 20 publications

Histopathological Findings of Cleft Palate in Rat Embryos Induced by Triamcinolone Acetonide

Histopathological Findings of Cleft Palate in Rat Embryos Induced by Triamcinolone Acetonide

Viable Ednra Y129F mice feature human mandibulofacial dysostosis with alopecia (MFDA) syndrome due to the homologue mutation

The effect of reducing ATP levels on reorientation of the secondary palate

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