Maternal diabetes induces senescence and neural tube defects sensitive to the senomorphic rapamycin
Cheng Xu, Wei-Bin Shen, E. Albert Reece, Hidetoshi Hasuwa, Christopher Harman, Sunjay Kaushal, Peixin Yang
Abstract
; transgenic expression of the dominant-negative FoxO3a mutant; or the senomorphic rapamycin. Double transgenic expression of p21 and p27 mimicked maternal diabetes in inducing premature neuroepithelium senescence and NTDs. These findings integrate transcription- and epigenome-regulated miRNAs and cell cycle regulators in premature neuroepithelium senescence and provide a mechanistic basis for targeting premature senescence and NTDs using senomorphics.
Topics & Concepts
Neural tubeSenescenceNeuroepithelial cellDiabetes mellitusCell biologyTube (container)microRNAOrganogenesisBiologyNeuroscienceChemistryNeural stem cellEndocrinologyMaterials scienceEmbryoGeneticsStem cellGeneComposite materialTelomeres, Telomerase, and SenescenceMicroRNA in disease regulationRNA regulation and disease