4.7 Article

Novel investigations in retinoic-acid-induced cleft palate about the gut microbiome of pregnant mice

Journal

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fcimb.2022.1042779

Keywords

cleft palate; retinoic acid; gut microbiome; lactobacillus; metabolism

Funding

  1. National Natural Science Foundation of China
  2. Excellent Talents in Dongcheng District of Beijing [81570940, 81873706, 82170912]
  3. Discipline Construction Fund from the Beijing Stomatological Hospital, School of Stomatology, Capital Medical University [2019DCT-M-23]
  4. [19-09-02]

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The study found that changes in maternal gut microbiome may affect the development of the palate, which is related to changes in Lactobacillus. These results provide a new direction in the pathogenesis of RA-induced cleft palate.
IntroductionCleft palate (CP) is one of the most common congenital birth defects in the craniofacial region, retinoic acid (RA) gavage is the most common method for inducing cleft palate model. Although several mechanisms have been proposed to illuminate RA-induced cleft palate during embryonic development, these findings are far from enough. Many efforts remain to be devoted to studying the etiology and pathogenesis of cleft palate. Recent research is gradually shifting the focus to the effect of retinoic acid on gut microbiota. However, few reports focus on the relationship between the occurrence of CP in embryos and gut microbiota. MethodsIn our research, we used RA to induce cleft palate model for E10.5 the feces of 5 RA-treated pregnant mice and 5 control pregnant mice were respectively metagenomics analysis. ResultsCompared with the control group, Lactobacillus in the gut microbiome the RA group was significantly increased. GO, KEGG and CAZy analysis of differentially unigenes demonstrated the most abundant metabolic pathway in different groups, lipopolysaccharide biosynthesis, and histidine metabolism. DiscussionOur findings indicated that changes in the maternal gut microbiome palatal development, which might be related to changes in Lactobacillus and These results provide a new direction in the pathogenesis of CP induced by RA.

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