ArticleInternational journal of clinical and experimental pathology2015
Molecular mechanism of Hoxd13-mediated congenital malformations in rat embryos.
Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the molecular mechanism of Hoxd13-mediated congenital malformations in rat embryos.
methodsSD female rats were mated with male rats in a 1:1 mating scheme. Thirty pregnant female rats were randomly divided into three groups: the control group receiving a normal diet, the model group receiving a vitamin A-deficient diet, and the treatment group receiving a vitamin A-deficient diet supplemented with pcDNA-Hoxd13. The expression of Hoxd13 mRNA and protein in normal embryonic tissue and congenital malformations was determined by RT-PCR and Western blot analysis. At day 20, rats were dissected, and the fetal weight, body and tail length, and the number of live births, absorbed fetus, and stillbirth in each group were recorded. Wnt and Slim1 expression was detected by RT-PCR and Western blot analysis. β-catenin and c-myc expression was also quantified by Western blot analysis.
resultsThe expression of Hoxd13 mRNA and protein in congenital malformations was significantly lower compared with normal embryonic tissue (P<0.01). The administration of exogenous Hoxd13 in the treatment group markedly increased the fetal weight, body and tail length (P<0.05), improved the embryonic survival rate, and reduced the embryonic resorption rate and stillbirth rate (P<0.05). Exogenous Hoxd13 markedly promoted the expression of Wnt2, Wnt5a, Wnt7b and Slim1 protein and mRNA (P<0.01), and the expression of β-catenin and c-myc protein in congenital malformations (P<0.01).
conclusionHoxd13 expression was decreased in rat embryos with congenital malformations. The administration of exogenous Hoxd13 alleviated fetal malformation probably through stimulation of Slim1 expression and Wnt/β-catenin signaling pathway.
Indexed as
Identifiers
26884828PMC4730041W2411532769What OpenQuestion holds
Registered trials
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