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Determination01:51

Determination

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During embryogenesis, cells become progressively committed to different fates through a two-step process: specification followed by determination. Specification is demonstrated by removing a segment of an early embryo, “neutrally” culturing the tissue in vitro—for example, in a petri dish with simple medium—and then observing the derivatives. If the cultured region gives rise to cell types that it would normally generate in the embryo, this means that it is specified. In...
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  11. Transcriptome Heterogeneity Of Congenital Cleft Palate Model In Congener New Zealand Rabbits Induced By Dexamethasone.
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  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Transcriptome Heterogeneity Of Congenital Cleft Palate Model In Congener New Zealand Rabbits Induced By Dexamethasone.

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Transcriptome heterogeneity of congenital cleft palate model in congener New Zealand rabbits induced by dexamethasone.

Lanling Lin1, Haoyue Liu1, Xiao Luo1

  • 1State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Dept. of Cleft Lip and Palate Surgery, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.

Hua Xi Kou Qiang Yi Xue Za Zhi = Huaxi Kouqiang Yixue Zazhi = West China Journal of Stomatology
|April 10, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Dexamethasone exposure in pregnant rabbits caused congenital cleft palate in offspring. Gene expression analysis revealed altered ARHGEF6, APC, and ABI2 levels, suggesting their role in this condition.

Keywords:
congenital cleft palatecytoskeleton regulationdexamethasonetranscriptomic analysis

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Area of Science:

  • Developmental Biology
  • Genetics
  • Pharmacology

Background:

  • Congenital cleft palate is a common birth defect with complex etiology.
  • Dexamethasone is a known teratogen that can induce cleft palate in animal models.
  • Understanding the molecular mechanisms is crucial for prevention and treatment strategies.

Purpose of the Study:

  • To investigate transcriptome heterogeneity in dexamethasone-induced congenital cleft palate in New Zealand rabbits.
  • To identify molecular mechanisms underlying cleft palate development.
  • To analyze gene expression differences between affected and unaffected offspring.

Main Methods:

  • Dexamethasone was administered to pregnant New Zealand rabbits during a critical gestational period.
  • Offspring were phenotyped for cleft palate.
  • RNA sequencing was performed on palatal tissues from cleft palate (CP) and non-cleft palate (NCP) groups.
  • Gene expression data were analyzed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses.
  • Real-time polymerase chain reaction (PCR) validated key gene expression changes.

    • Main Results:

    • 225 differentially expressed genes were identified between CP and NCP groups (120 upregulated, 105 downregulated).
    • Significant enrichment was observed in GO terms including heterotrimeric G protein complex and extracellular matrix.
    • KEGG analysis revealed enrichment in pathways such as regulation of actin cytoskeleton, GABAergic synapse, and Apelin signaling pathway.
    • ARHGEF6 and ABI2 gene expression decreased, while APC gene expression increased in the CP group compared to NCP.

    Conclusions:

    • Abnormal expression of ARHGEF6, APC, and ABI2 genes, involved in actin cytoskeleton regulation, is associated with dexamethasone-induced congenital cleft palate in rabbits.
    • These findings provide insights into the molecular pathogenesis of cleft palate.
    • The study highlights potential targets for future therapeutic interventions.