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Effect of depletion of TCF23 on myometrium transcriptome profile during late pregnancy

ABSTRACT: TCF23 is a basic-helix-loop-helix transcription factor lacking a DNA binding domain with a C-terminal mediated inhibitory action. Tcf23 was significantly induced by progesterone but not estradiol in vitro and in vivo. To evaluate the biological role of Tcf23, we generated the Tcf23 knockout mouse. Although pregnant Tcf23 KO mice were able to maintain gestation until full term, a considerable proportion of KO females experienced delayed parturition, dystocia, and reduced litter outcomes, with a high incidence of resorption and fetal lethality. Morphological analysis of the pregnant uterus revealed aberrant disruption of both circular and longitudinal myometrial layers and disarrayed extracellular matrix at the conceptus sites in the KO mice. Transcriptome profile analysis of the KO myometrium demonstrated disruptions in cell adhesion, extracellular matrix (ECM), and gap junction signaling, indicating the crucial role of TCF23 in myometrial remodeling and preparation for contractility during late pregnancy. Altogether, our research highlights a novel cause for labor dysfunction mediated by loss of Tcf23 activity in murine uterine tissue.

ORGANISM(S): Mus musculus

PROVIDER: GSE236861 | GEO | 2024/04/01

REPOSITORIES: GEO

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Project description:The process of parturition involves the complex interplay of factors that changes the excitability and contractile activity of the uterus. We have compared the relative gene expression profile of myometrium from rats before parturition (21 days pregnant) and during delivery using high-density DNA microarray. Of 8740 sequences available in the array a total of 3782 were detected as present. From the sequences that were significantly altered, 59 genes were upregulated and 82 genes were downregulated. We were able to detect changes in genes described to have altered expression level at term including connexin 43 and 26, cyclo-oxygenase 2 and oxytocin receptor as well as novel genes that have been not previously associated with parturition. Quantitative real time PCR on selected genes further confirmed the microarray data. Here we report for the first time that aquaporin5 (AQP5), a member of aquaporin (AQP) water channel family, was dramatically downregulated during parturition (~100 fold by microarray and ~50 fold by Real Time PCR). The emerging profile highlights biochemical cascades occurring in a period of about 36 hours that triggers parturition and the initiation of myometrium reverse remodeling after partum. The microarray analysis uncovered genes that were previously suspected to play a role in parturition. This regulation involves genes from immune/inflammatory response, steroid/lipids metabolism, calcium homeostasis, cell volume regulation, cell signaling, cell division, and tissue remodeling, suggesting the presence of multiple and redundant mechanisms altered in the process of birth. Experiment Overall Design: Uteri were dissected from late pregnant rats (21 days, LP) (three individuals, two replicates of sample 1) and rats during labor (DL) after the expulsion of the second pup (three individuals, two replicates of sample 1). After dissection, uteri were placed immediately in cold Ca2+-free PBS buffer and peripheral large blood vessels, external surrounding connective tissue and placenta were removed. The endometrium superficial layer was separated by gentle scraping. The myometrium was weighted, finely minced and homogenized with a polytron (Polytron PT3000, Brinkmann, Switzerland).

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Effect of depletion of TCF23 on myometrium transcriptome profile during late pregnancy

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