ArticleReproductive biology and endocrinology : RB&E2006
Sexually dimorphic gene expression that overlaps maturation of type II pneumonocytes in fetal mouse lungs.
Article in Reproductive biology and endocrinology : RB&E, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 20 citations in OpenAlex.
- Unusual X chromosome inactivation maintenance in female alveolar type 2 cells is correlated with increased numbers of X-linked escape genes and sex-biased gene expression.Stem cell reports · 2023Article
- Ultrasonographic changes in fetal gastrointestinal motility during the last ten days before parturition in dogs.Frontiers in veterinary science · 2022Article
- Deletion of hypoxia-responsive microRNA-210 results in a sex-specific decrease in nephron number.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Expression profile of androgen-modulated microRNAs in the fetal murine lung.Biology of sex differences · 2016Article
- Article
- Identification of most stable endogenous control genes for microRNA quantification in the developing mouse lung.PloS one · 2014Article
- Apolipoprotein A-I, A-II, and H mRNA and protein accumulation sites in the developing lung in late gestation.BMC research notes · 2011Article
- Gene expression profile of androgen modulated genes in the murine fetal developing lung.Reproductive biology and endocrinology : RB&E · 2010Article
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3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundIn human, respiratory distress of the neonates, which occurs in prematurity, is prevalent in male. Late in gestation, maturation of type II pneumonocytes, and consequently the surge of surfactant synthesis are delayed in male fetuses compared with female fetuses. Although the presence of higher levels of androgens in male fetuses is thought to explain this sex difference, the identity of genes involved in lung maturation that are differentially modulated according to fetal sex is unknown. We have studied the sex difference in developing mouse lung by gene profiling during a three-day gestational window preceding and including the emergence of mature PTII cells (the surge of surfactant synthesis in the mouse occurs on GD 17.5).
methodsTotal RNA was extracted from lungs of male and female fetal mice (gestation days 15.5, 16.5, and 17.5), converted to cRNA, labeled with biotin, and hybridized to oligonucleotide microarrays (Affymetrix MOE430A). Analysis of data was performed using MAS5.0, LFCM and Genesis softwares.
resultsMany genes involved in lung maturation were expressed with no sex difference. Of the approximative 14,000 transcripts covered by the arrays, only 83 genes presented a sex difference at one or more time points between GDs 15.5 and 17.5. They include genes involved in hormone metabolism and regulation (i.e. steroidogenesis pathways), apoptosis, signal transduction, transcriptional regulation, and lipid metabolism with four apolipoprotein genes. Genes involved in immune functions and other metabolisms also displayed a sex difference.
conclusionAmong these sexually dimorphic genes, some may be candidates for a role in lung maturation. Indeed, on GD 17.5, the sex difference in surfactant lipids correlates with the sex difference in pulmonary expression of apolipoprotein genes, which are involved in lipid transport. This suggests a role for these genes in the surge of surfactant synthesis. Our results would help to identify novel genes involved in the physiopathology of the respiratory distress of the neonates.
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