Dexamethasone Effect on Embryonic Chick Respiratory Epithelium

1982 ◽  
Vol 40 ◽  
pp. 248-249
Author(s):  
M.R. Richter ◽  
R.V. Blystone
Keyword(s):  
Lung Development ◽  
Critical Role ◽  
Respiratory Epithelium ◽  
Chick Embryos ◽  
Embryonic Chick ◽  
White Leghorn ◽  
Lung Maturation ◽  
Synthetic Analogs ◽  
Lung Physiology ◽  
Avian Lung

Dexamethasone and other synthetic analogs of corticosteroids have been employed clinically as enhancers of lung development. The mechanism(s) by which this steroid induction of later lung maturation operates is not clear. This study reports the effect on lung epithelia of dexamethasone administered at different intervals during development. White Leghorn chick embryos were used so as to remove possible maternal and placental influences on the exogenously applied steroid. Avian lung architecture does vary from mammals; however, respiratory surfactant produced by the lung epithelia serves an equally critical role in avian lung physiology.

Effects of hypoxia or hyperoxia on the lung of the chick embryo

1989 ◽  
Vol 67 (5) ◽  
pp. 515-519 ◽  
Author(s):  
Lijing Xu ◽  
Jacopo P. Mortola
Keyword(s):  
Chick Embryo ◽  
Lung Development ◽  
Chronic Hypoxia ◽  
Ventilatory Response ◽  
Mechanical Stretch ◽  
Mechanical Effect ◽  
Cellular Component ◽  
Chick Embryos ◽  
Breathing Cycle ◽  
Avian Lung

Newborn mammals in chronic hypoxia or hyperoxia experience, respectively, an increase or decrease in lung weight:body weight ratios, possibly because of the mechanical effect on the lung accompanying the ventilatory response. Because the avian lung does not expand or contract with the breathing cycle, we asked whether or not qualitatively similar changes could be observed in the lung of chick embryos incubated in hypoxic or hyperoxic conditions. Hypoxic embryos (10% O2, days 14–18) were smaller than controls incubated in normoxia, with higher hematocrit values and larger lung weight:body weight ratios (both wet and dry). Both the total pulmonary DNA (reflecting the cellular component) and the DNA concentration were decreased in hypoxia. Hyperoxic embryos (50% O2, days 7–18 or days 14–18) had lower hematocrit values and smaller dry lung weight:body weight ratios than controls, with similar DNA concentrations. In general, the differences from controls were more apparent in those embryos hyperoxic from day 14 to 18 of incubation than from day 7 to 18. We conclude that changes in lung weights qualitatively similar to those occurring in the chronically hypoxic or hyperoxic newborn mammal can also be observed in the hypoxic or hyperoxic chick embryo, suggesting that they are not necessarily caused by changes in mechanical stretch on the lung.Key words: lung development, lung DNA, avian growth.

scholarly journals Molecular regulation of lung maturation in near-term fetal sheep by maternal daily vitamin C treatment in late gestation

2021 ◽  
Author(s):  
Erin V. McGillick ◽  
Sandra Orgeig ◽  
Beth J. Allison ◽  
Kirsty L. Brain ◽  
Youguo Niu ◽  
...  
Keyword(s):  
Vitamin C ◽  
Lung Development ◽  
Fetal Lung ◽  
Late Gestation ◽  
Lung Maturation ◽  
Maternal Vitamin ◽  
Healthy Pregnancy ◽  
Daily Vitamin ◽  
Expression Of Genes ◽  
Fetal Lung Maturation

Abstract Background In the fetus, the appropriate balance of prooxidants and antioxidants is essential to negate the detrimental effects of oxidative stress on lung maturation. Antioxidants improve respiratory function in postnatal life and adulthood. However, the outcomes and biological mechanisms of antioxidant action in the fetal lung are unknown. Methods We investigated the effect of maternal daily vitamin C treatment (200 mg/kg, intravenously) for a month in late gestation (105–138 days gestation, term ~145 days) on molecular regulation of fetal lung maturation in sheep. Expression of genes and proteins regulating lung development was quantified in fetal lung tissue. The number of surfactant-producing cells was determined by immunohistochemistry. Results Maternal vitamin C treatment increased fetal lung gene expression of the antioxidant enzyme SOD-1, hypoxia signaling genes (HIF-2α, HIF-3α, ADM, and EGLN-3), genes regulating sodium movement (SCNN1-A, SCNN1-B, ATP1-A1, and ATP1-B1), surfactant maturation (SFTP-B and ABCA3), and airway remodeling (ELN). There was no effect of maternal vitamin C treatment on the expression of protein markers evaluated or on the number of surfactant protein-producing cells in fetal lung tissue. Conclusions Maternal vitamin C treatment in the last third of pregnancy in sheep acts at the molecular level to increase the expression of genes that are important for fetal lung maturation in a healthy pregnancy. Impact Maternal daily vitamin C treatment for a month in late gestation in sheep increases the expression of gene-regulating pathways that are essential for normal fetal lung development. Following late gestation vitamin C exposure in a healthy pregnancy, an increase in lung gene but not protein expression may act as a mechanism to aid in the preparation for exposure to the air-breathing environment after birth. In the future, the availability/development of compounds with greater antioxidant properties than vitamin C or more specific targets at the site of oxidative stress in vivo may translate clinically to improve respiratory outcomes in complicated pregnancies at birth.

Suppression of cell proliferation and programmed cell death by dexamethasone during postnatal lung development

2002 ◽  
Vol 282 (3) ◽  
pp. L477-L483 ◽  
Author(s):  
Cédric Luyet ◽  
Peter H. Burri ◽  
Johannes C. Schittny
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Lung Development ◽  
Structural Changes ◽  
Tissue Transglutaminase ◽  
Lung Parenchyma ◽  
Lung Maturation ◽  
Morphological Criteria ◽  
Postnatal Lung Development

Prematurely born babies are often treated with glucocorticoids. We studied the consequences of an early postnatal and short dexamethasone treatment (0.1–0.01 μg/g, days 1–4) on lung development in rats, focusing on its influence on peaks of cell proliferation around day 4 and of programmed cell death at days 19–21. By morphological criteria, we observed a dexamethasone-induced premature maturation of the septa ( day 4), followed by a transient septal immatureness and delayed alveolarization leading to complete rescue of the structural changes. The numbers of proliferating (anti-Ki67) and dying cells (TdT-mediated dUTP nick end labeling) were determined and compared with controls. In dexamethasone-treated animals, both the peak of cell proliferation and the peak of programmed cell death were reduced to baseline, whereas the expression of tissue transglutaminase (transglutaminase-C), another marker for postnatal lung maturation, was not significantly altered. We hypothesize that a short neonatal course of dexamethasone leads to severe but transient structural changes of the lung parenchyma and influences the balance between cell proliferation and cell death even in later stages of lung maturation.

scholarly journals Loss of potassium from embryonic chick hearts in potassium-free media with and without calcium

1938 ◽  
Vol 124 (837) ◽  
pp. 446-450
Keyword(s):  
Phosphate Buffer ◽  
Direct Evidence ◽  
Watch Glass ◽  
Chick Embryos ◽  
Embryonic Chick ◽  
Intercellular Spaces ◽  
Experimental Solution ◽  
Free Media ◽  
And Control ◽  
Day By Day

Experiments already described (Murray 1938) led to the inference that the cells of the chick embryonic heart lose potassium in potassium-free media. The experiments here described provide direct evidence of this. The hearts were dissected out of 2 ½-3 day chick embryos and placed in the solution PC (Table I) until they had started to beat. They were then thoroughly washed, and were allowed to lie for 5 min. (2 min. in Exp. 1) in the last wash. This last wash is called control A. The solutions used for washing were from the same flasks as the experimental solution. After their passage through control A the hearts were transferred to 2 c.c. of the experimental solution in a Jena watch-glass. After various times in this the hearts were discarded and both the experimental solution and control A were collected. If the experiment extended over more than 1 day the experimental solution and control A were used over again day by day until all the hearts in the experiment had passed through them. The use of control A was necessary for two reasons: ( a ) to show that potassium was not still being washed out of the intercellular spaces at the end of washing ( b ) in experiments lasting over several days the washing solution was fresh each day, but the experimental solution was of course not changed. Hence any small amount of potassium being carried over from the last wash would accumulate in the experimental solution because of the daily increment and might seriously affect the result; but by leaving the hearts for several minutes in the last wash (control A) and by not changing it for fresh on successive days, any such increase would be detected in that solution. In addition to control A, a daily sample (control B) was taken from the same flasks as the solutions used for washing. Details of the solutions are given in Table I ; a phosphate buffer was always used.

Thyroid hormone effects on chick scale morphogenesis and keratinization

Development ◽  
1970 ◽  
Vol 24 (1) ◽  
pp. 65-71
Author(s):  
Nancy K. Lawrenz ◽  
Leland G. Johnson
Keyword(s):  
Thyroid Hormone ◽  
Scale Development ◽  
New Hampshire ◽  
Chick Embryos ◽  
White Leghorn ◽  
Endocrine Effects ◽  
Hormone Effects ◽  
Hormone Responsiveness

The effects of thiourea injection on scale development were studied in New Hampshire Red × White Leghorn Cross chick embryos. Normal morphogenesis and keratinization of scales were significantly delayed in thioureatreated specimens. Subsequent thyroxine injection resulted in normal or even precocious scale development. The thyroid hormone responsiveness of scale development is discussed in relation to other studies of endocrine effects on differentiation of skin and skin derivatives.

The genesis of membrane bone in the embryonic chick maxilla: epithelial-mesenchymal tissue recombination studies

Development ◽  
1980 ◽  
Vol 56 (1) ◽  
pp. 269-281
Author(s):  
Mary S. Tyler ◽  
David P. McCobb
Keyword(s):  
Bone Formation ◽  
Hind Limb ◽  
Bone Grafts ◽  
Chick Embryos ◽  
Embryonic Chick ◽  
Limb Buds ◽  
Mesenchymal Tissue ◽  
Membrane Bone ◽  
Tissue Recombination

In the present study, the question of whether a relatively non-specific epithelial requirement exists for membrane bone formation within the maxillary mesenchyme was investigated. Organ rudiments from embryonic chicks of three to five days of incubation (HH 18–25) were enzymatically separated into the epithelial and mesenchymal components. Maxillarymesenchyme (from embryos HH 18–19) which in the absence of epithelium will not form bone was recombined with epithelium from maxillae of similarly aged embryos (homotypichomochronic recombination) and of older embryos (HH 25) (homotypic-heterochronicrecombination). Heterotypic recombinations were made between maxillary mesenchyme (HH 18–19) and the epithelium from wing and hind-limb buds (HH 19–22). Recombinants were grown as grafts on thechorioallantoic membranes of host chick embryos. Grafts of intact maxillae, isolated maxillary mesenchyme, and isolated epithelia from the maxilla, wing-, and hind-limb buds weregrown as controls. The histodifferentiation of grafted intact maxillae was similar to that in vivo; both cartilage and membrane bone differentiated within the mesenchyme. Grafts of maxillary mesenchyme (from embryos HH 18–19) grown in the absence of epithelium formed cartilage but did not form membrane bone. Grafts of maxillary mesenchyme (from embryos HH 18–19) recombined with epithelium in homotypichomochronic, homotypic-heterochronic, and heterotypic tissue combinations formed membrane bone in addition to cartilage. These results indicate that maxillary mesenchyme requires the presence of epithelium to promote osteogenesis and that this epithelial requirement is relatively non-specific in terms of type and age of epithelium.

Adenoviral E3-14.7K protein in LPS-induced lung inflammation

2000 ◽  
Vol 278 (4) ◽  
pp. L631-L639 ◽  
Author(s):  
Kevin S. Harrod ◽  
Amber D. Mounday ◽  
Jeffrey A. Whitsett
Keyword(s):  
Transgenic Mice ◽  
Lung Inflammation ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Respiratory Epithelium ◽  
Wild Type ◽  
Intracellular Staining ◽  
Intratracheal Administration ◽  
Tnf Α

The adenoviral E3-14.7K protein is a cytoplasmic protein synthesized after adenoviral infection. To assess the contribution of E3-14.7K-sensitive pathways in the modulation of inflammation by the respiratory epithelium, inflammatory responses to intratracheal lipopolysaccharide (LPS) and tumor necrosis factor (TNF)-α were assessed in transgenic mice bearing the adenoviral E3-14.7K gene under the direction of the surfactant protein (SP) C promoter. When E3-14.7K transgenic mice were administered LPS intratracheally, lung inflammation as indicated by macrophage and neutrophil accumulation in bronchoalveolar lavage fluid was decreased compared with wild-type control mice. Lung inflammation and epithelial cell injury were decreased in E3-14.7K mice 24 and 48 h after LPS administration. Intracellular staining for surfactant proprotein (proSP) B, proSP-C, and SP-B was decreased and extracellular staining was markedly increased in wild-type mice after LPS administration, consistent with LPS-induced lung injury. In contrast, intense intracellular staining of proSP-B, proSP-C, and SP-B persisted in type II cells of E3-14.7K mice, whereas extracellular staining of proSP-B and proSP-C was absent. Inhibitory effects of intratracheal LPS on SP-C mRNA were ameliorated by expression of the E3-14.7Kgene. Similar to the response to LPS, lung inflammation after intratracheal administration of TNF-α was decreased in E3-14.7K transgenic mice. Levels of TNF-α after LPS administration were similar in wild-type and E3-14.7K-bearing mice. Cell-selective expression of E3-14.7K in the respiratory epithelium inhibited LPS- and TNF-α-mediated lung inflammation, demonstrating the critical role of respiratory epithelial cells in LPS- and TNF-α-induced lung inflammation.

scholarly journals A critical role for miR-142 in alveolar epithelial lineage formation in mouse lung development

2019 ◽  
Vol 76 (14) ◽  
pp. 2817-2832 ◽  
Author(s):  
Amit Shrestha ◽  
Gianni Carraro ◽  
Nicolas Nottet ◽  
Ana Ivonne Vazquez-Armendariz ◽  
Susanne Herold ◽  
...  
Keyword(s):  
Lung Development ◽  
Critical Role ◽  
Mouse Lung ◽  
Alveolar Epithelial

scholarly journals Targeted Disruption of Mouse Dip2B Leads to Abnormal Lung Development and Prenatal Lethality

2020 ◽  
Vol 21 (21) ◽  
pp. 8223
Author(s):  
Rajiv Kumar Sah ◽  
Jun Ma ◽  
Fatoumata Binta Bah ◽  
Zhenkai Xing ◽  
Salah Adlat ◽  
...  
Keyword(s):  
Lung Development ◽  
Cell Types ◽  
Branching Morphogenesis ◽  
Brdu Incorporation ◽  
Mouse Lung ◽  
Alveolar Type ◽  
Type I ◽  
Lung Maturation ◽  
M Phase

Molecular and anatomical functions of mammalian Dip2 family members (Dip2A, Dip2B and Dip2C) during organogenesis are largely unknown. Here, we explored the indispensable role of Dip2B in mouse lung development. Using a LacZ reporter, we explored Dip2B expression during embryogenesis. This study shows that Dip2B expression is widely distributed in various neuronal, myocardial, endothelial, and epithelial cell types during embryogenesis. Target disruption of Dip2b leads to intrauterine growth restriction, defective lung formation and perinatal mortality. Dip2B is crucial for late lung maturation rather than early-branching morphogenesis. The morphological analysis shows that Dip2b loss leads to disrupted air sac formation, interstitium septation and increased cellularity. In BrdU incorporation assay, it is shown that Dip2b loss results in increased cell proliferation at the saccular stage of lung development. RNA-seq analysis reveals that 1431 genes are affected in Dip2b deficient lungs at E18.5 gestation age. Gene ontology analysis indicates cell cycle-related genes are upregulated and immune system related genes are downregulated. KEGG analysis identifies oxidative phosphorylation as the most overrepresented pathways along with the G2/M phase transition pathway. Loss of Dip2b de-represses the expression of alveolar type I and type II molecular markers. Altogether, the study demonstrates an important role of Dip2B in lung maturation and survival.

scholarly journals Effects of leptin deficiency on postnatal lung development in mice

2008 ◽  
Vol 105 (1) ◽  
pp. 249-259 ◽  
Author(s):  
Kewu Huang ◽  
Richard Rabold ◽  
Eric Abston ◽  
Brian Schofield ◽  
Vikas Misra ◽  
...  
Keyword(s):  
Surface Area ◽  
Morphometric Analysis ◽  
Lung Development ◽  
Age Groups ◽  
Lung Parenchyma ◽  
Lung Maturation ◽  
Alveolar Surface Area ◽  
Leptin Deficiency ◽  
Postnatal Lung Development ◽  
Alveolar Surface

Leptin modulates energy metabolism and lung development. We hypothesize that the effects of leptin on postnatal lung development are volume dependent from 2 to 10 wk of age and are independent of hypometabolism associated with leptin deficiency. To test the hypotheses, effects of leptin deficiency on lung maturation were characterized in age groups of C57BL/6J mice with varying Lep ob genotypes. Quasi-static pressure-volume curves and respiratory impedance measurements were performed to profile differences in respiratory system mechanics. Morphometric analysis was conducted to estimate alveolar size and number. Oxygen consumption was measured to assess metabolic rate. Lung volume at 40-cmH2O airway pressure (V40) increased with age in each genotypic group, and V40 was significantly ( P < 0.05) lower in leptin-deficient ( ob/ ob) mice beginning at 2 wk. Differences were amplified through 7 wk of age relative to wild-type (+/+) mice. Morphometric analysis showed that alveolar surface area was lower in ob/ ob compared with +/+ and heterozygote ( ob/+) mice beginning at 2 wk. Unlike the other genotypic groups, alveolar size did not increase with age in ob/ ob mice. In another experiment, ob/ ob at 4 wk received leptin replacement (5 μg·g−1·day−1) for 8 days, and expression levels of the Col1a1, Col3a1, Col6a3, Mmp2, Tieg1, and Stat1 genes were significantly increased concomitantly with elevated V40. Leptin-induced increases in V40 corresponded with enlarged alveolar size and surface area. Gene expression suggested a remodeling event of lung parenchyma after exogenous leptin replacement. These data support the hypothesis that leptin is critical to postnatal lung remodeling, particularly related to increased V40 and enlarged alveolar surface area.

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