Animals ; Brain ; embryology ; Ear ; embryology ; Esophagus ; embryology ; Fallopian Tubes ; embryology ; Female ; Heart ; embryology ; Humans ; Kidney ; embryology ; Liver ; embryology ; Lung ; embryology ; Male ; Organogenesis ; physiology ; Penis ; embryology ; Rabbits ; Stomach ; embryology ; Vagina ; embryology

Animals ; Bronchopulmonary Dysplasia ; etiology ; Fibroblasts ; physiology ; Humans ; Hyperoxia ; pathology ; Infant, Newborn ; Lung ; embryology ; pathology

OBJECTIVEThis study aimed to explore the effects of hyperoxia on the development of fetal lung by investigating the changes of morphological and cell proliferation induced by hyperoxia in cultured fetal lungs as well as the effects of dexamethasone on hyperoxia-exposed lungs.

METHODSHuman fetal lung explants at the pseudoglandular stage of development were cultured randomly either in normoxia (21% O2/5% CO2) or hyperoxia (95% O2/5% CO2) for 72 hrs. Dexamethasone was added into the feeding medium at the concentration of 10(-6)M. Harvested tissues were stained for pancytokeratin to identify epithelial cells, with Ki-67 as a marker of proliferation. The effects of lung morphometry were analyzed using computer assisted image analysis. The mean airway thickness, the proportion of the surface area occupied by airways, the mean airway surface area and the index of the epithelium proliferation were measured.

RESULTSThe lung architectures remained unchanged after 72 hrs normoxia culture, whereas hyperoxia culture resulted in significant dilation of airways and thinning of epithelium, with the surface area of airways of 6662 microm(2) vs 2728 microm(2) and the thickness of airways of 7.8 microm vs 8.1 microm (P < 0.05). Hyperoxia culture also resulted in an increase in the proportion of the surface area occupied by airways than normoxia culture (35.2% vs 23.4%; P < 0.05). The surface area of airways (3174 microm(2)) and the proportion of the surface area occupied by airways (23.9%) decreased significantly in hyperoxia-cultured lungs after dexamethasone administration (P < 0.05). The epithelium proliferation index in hyperoxia-cultured lungs (21.8%) was higher than that in normoxia-cultured lungs (5.1%) and dexamethasone-treated hyperoxia-cultured lungs (7.4%) (P < 0.05).

CONCLUSIONSThe exposure of pseudoglandular lungs to hyperoxia modulates the lung architecture to resemble saccular lungs with higher epithelium proliferation index. Dexamethasone may inhibit the effects induced by hyperoxia.

Cell Differentiation ; drug effects ; Dexamethasone ; pharmacology ; Female ; Humans ; Hyperoxia ; pathology ; Lung ; drug effects ; embryology ; pathology ; Pregnancy

OBJECTIVEMany studies have shown that tissue development is closely correlated with fluid transport. Aquaporins (AQPs) are a group of cell membrane proteins that actively and selectively transport water. This study aimed to investigate the changes of AQPs expression during lung development in rats in order to elucidate the role of AQPs in the rat lung development.

METHODSAQP1, AQP3, AQP4 and AQP5 proteins and mRNA in the lung cell membrane were measured by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) respectively in the 20-day-old embryo (E20), 7-day-old newborn rat, and one-month-old young and adult rats. The correlation between AQPs expression and lung development was studied.

RESULTSWith increasing age, the lung development showed a dynamic and successive course, with the most rapid from the fetus to the newborn rat, and then a slowed down afterwards. AQPs mRNA was weakly expressed in the lung of the E20 group. Lung AQPs mRNA and protein increased rapidly after birth until adulthood. The AQPs distribution patterns in the lung were unique with no duplication. There was a positive correlation between AQPs expression and lung development (P<0.05).

CONCLUSIONSIn addition to being involved in the transepithelial transport of water in the lung, AQPs is also related to its development.

Animals ; Aquaporins ; analysis ; genetics ; physiology ; Immunohistochemistry ; Lung ; embryology ; metabolism ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar

OBJECTIVETo study the effect of maternal vitamin D deficiency on lung morphogenesis and platelet-derived growth factor-A (PDGF-A) expression in rat offspring.

METHODSSprague-Dawley (SD) female rats were randomly divided into two groups: normal control and vitamin D deficiency, with 6 rats in each group. The vitamin D deficiecy group was kept away from light and fed with the forage without vitamin D. After 2 weeks, the rats were mated with normal SD male rats. The morphological changes of fetal rat lungs on day 20 of gestation and 1-day-old neonatal rat lungs were observed by light microscope and electronic microscope. The levels of PDGF-A mRNA and protein in fetal and neonatal rat lungs were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) technique and Western blot method respectively.

RESULTSUnder the light microscope, smaller alveolar space, smaller diameter of the respiratory membrane and thicker alveolus mesenchyma were observed in lungs of fetal and neonatal rats from the vitamin D deficiency group compared with the controls (P<0.05). Under the electronic microscope, fewer lamellar bodies but more glycogen deposition in intracytoplasm were observed in the lungs of fetal rats from the vitamin D deficiency group compared with the controls. There was an increased number of empty lamellar bodies in neonatal rats from the vitamin D deficiency group. The levels of PDGF-A mRNA and protein in lungs of fetal and neonatal rats from the vitamin D deficiency group were significantly lower than the controls (P<0.05).

CONCLUSIONSMaternal vitamin D deficiency during pregnancy may inhibit the development of lung morphogenesis and PDGF-A expression in late fetal and neonatal rats. The low expression of PDGF-A may be involved in the inhibitory effect of vitamin D deficiency on the lung development.

Animals ; Calcifediol ; blood ; Female ; Lung ; embryology ; pathology ; ultrastructure ; Platelet-Derived Growth Factor ; analysis ; genetics ; metabolism ; Pregnancy ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley ; Vitamin D Deficiency ; embryology ; metabolism

Cytoplasmic Cu/Zn superoxide dismutase (SOD1) is an antioxidant enzyme that converts superoxide to hydrogen peroxide in cells. Its spatial distribution matches that of superoxide production, allowing it to protect cells from oxidative stress. SOD1 deficiencies result in embryonic lethality and a wide range of pathologies in mice, but little is known about normal SOD1 protein expression in developing embryos. In this study, the expression pattern of SOD1 was investigated in post-implantation mouse embryos and extraembryonic tissues, including placenta, using Western blotting and immunohistochemical analyses. SOD1 was detected in embryos and extraembryonic tissues from embryonic day (ED) 8.5 to 18.5. The signal in embryos was observed at the lowest level on ED 9.5-11.5, and the highest level on ED 17.5-18.5, while levels remained constant in the surrounding extraembryonic tissues during all developmental stages examined. Immunohistochemical analysis of SOD1 expression on ED 13.5-18.5 revealed its ubiquitous distribution throughout developing organs. In particular, high levels of SOD1 expression were observed in the ependymal epithelium of the choroid plexus, ganglia, sensory cells of the olfactory and vestibulocochlear epithelia, blood cells and vessels, hepatocytes and hematopoietic cells of the liver, lymph nodes, osteogenic tissues, and skin. Thus, SOD1 is highly expressed at late stages of embryonic development in a cell- and tissue-specific manner, and can function as an important antioxidant enzyme during organogenesis in mouse embryos.
Animals ; Cerebral Cortex/embryology/enzymology ; Copulation ; Cytoplasm/*enzymology ; Embryonic Development/*physiology ; Female ; Immunohistochemistry ; Lung/embryology/enzymology ; Male ; Mice ; Mice, Inbred ICR ; Organogenesis/*physiology ; Pregnancy ; Stomach/embryology/enzymology ; Superoxide Dismutase/deficiency/genetics/*metabolism

The aberrant epigenetic reprogramme is an important cause for abnormal development of nuclear transfer embryos. The objective of this study was to investigate the CpG island methylation profiles and relative expression levels of H19 gene in different tissues of cloned goat fetus. We detected liver, placenta, kidney, lung and heart in the dead cloned goat fetus and the age-matched normal goat fetus (control) by using bisulfite sequencing and real time PCR. Results indicated that methylation levels of the fifth CpG island of H19 gene in dead cloned goat fetus was significant high compared with that in the control in placenta (70% vs 49.41%, P < 0.05), and relative expression levels of H19 gene was significant low compared with that in the control (883.3 vs 1 264.5, P < 0.05). Reversely, the methylation levels was significant low compared with that in the control in lung (63.53% vs 88.24%, P < 0.05), and relative expression levels was significant high compared with that in the control (1 003.4 vs 515.5, P < 0.05). The differences of others groups were insignificant (P > 0.05). Results showed the abnormal DNA methylation proflies of H19 gene occurred in some tissues of cloned goat fetus, which affected normal expression levels of H19 gene, indicating that aberrant DNA methylation reprogramme may be one of the important factors for the death of cloned animals.
Animals ; Cloning, Organism ; veterinary ; CpG Islands ; DNA Methylation ; Epigenesis, Genetic ; Female ; Fetus ; metabolism ; Genomic Imprinting ; Goats ; Kidney ; embryology ; metabolism ; Liver ; embryology ; metabolism ; Lung ; embryology ; metabolism ; Nuclear Transfer Techniques ; RNA, Long Noncoding ; RNA, Untranslated ; genetics ; metabolism

OBJECTIVETo bioinformatically predict and analyze target genes of miRNA-126(*), with the aim of providing certain basis for related research about target genes and regulatory mechanism in the future.

METHODSThe miRNA chip technology was applied to measure expression levels of miRNA-126(*) in 3 time points (embryo 16, 19 and 21 days) of fetal lung development. Then the target genes of miRNA-126(*) were screened through miRGen2.0 database. Subsequent bioinformatic analysis of these target genes was performed by Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes Pathway analysis (KEGG Pathway analysis).

RESULTSmiRNA-126(*) manifested continuously upregulated expression with the lung development (from embryo 16 to 21 days). There were 422 predicted target genes in total, and the gene set mainly located in glucuronosyltransferase activity, transferase activity (GO molecular function), multicellular organismal development, developmental process (GO biology process) and intracellular part (GO cellular component). The KEGG Pathway analysis demonstrated that the gene set mostly located in RNA degradation (signal transduction pathway) and prion diseases (disease pathway).

CONCLUSIONSThe results suggest that miRNA-126(*) plays a certain role in fetal lung development and provide a basis for lung development research in the future.

Animals ; Computational Biology ; Female ; Glucuronosyltransferase ; metabolism ; Lung ; embryology ; Male ; MicroRNAs ; physiology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; physiology

OBJECTIVETo investigate the expression and role of miRNA-126/miRNA-126(*) in the fetal lung development of rats.

METHODSTwelve pregnant Sprague-Dawley rats were randomly divided into 3 groups and the fetal rats were removed at 16, 19 and 21 days of gestation respectively. Hematoxylin and eosin staining was performed to observe lung morphology of fetal rats. Then microRNA (miRNA) microarray was used to study the expression patterns of miRNA-126/miRNA-126(*) in fetal lungs at the three time points. And miRNA-126(*) was selected for further study by real-time PCR.

RESULTSThere was no evident difference in the expression of miRNA-126 among the three groups, however the expression level of miRNA-126(*) increased gradually as the fetal lung developed. The real-time PCR result further showed that expression of miRNA-126(*) increased gradually with lung development, displaying significant differences among the three groups (P<0.05).

CONCLUSIONSmiRNA-126(*) may play an important role in development of the fetal lung in rats.

Animals ; Female ; Lung ; embryology ; Male ; MicroRNAs ; analysis ; physiology ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction

The development and evolution of fetal surgery and the recognition of the fetus as a patient came from two sources. First, were those obstetricians and perinatologists who detected life threatening anomalies before birth, and re-described a hidden mortality arising from death in utero. Ultrasonography, color Doppler ultrasound and ultrafast fetal magnetic resonance imaging have since enhanced the accuracy of prenatal evaluation. Second, were those pediatricians responsible for treating newborn infants with extremely serious problems, and that appeared untreatable, although, it was believed that they could have been treated at an earlier stage of development. After the natural history of several correctable lesions had been determined and the selection criteria for intervention developed, fetal surgery emerged as a means of improving the overall morbidity and mortality rates.
Cystic Adenomatoid Malformation of Lung, Congenital/surgery ; Fetal Diseases/*surgery ; Fetus/*surgery ; Hernia, Diaphragmatic/congenital/surgery ; Human ; Postoperative Care ; Preoperative Care ; Sacrococcygeal Region ; Spinal Neoplasms/embryology/surgery ; Teratoma/embryology/surgery