Early postnatal lung development in the eastern quoll ( Dasyurus viverrinus)

2021 ◽  
Author(s):  
Kirsten Ferner
Keyword(s):  
Lung Development ◽  
Postnatal Lung Development

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.

Expression of epidermal growth factor and surfactant proteins during postnatal and compensatory lung growth

2002 ◽  
Vol 283 (5) ◽  
pp. L981-L990 ◽  
Author(s):  
David J. Foster ◽  
Xiao Yan ◽  
Dennis J. Bellotto ◽  
Orson W. Moe ◽  
Herbert K. Hagler ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Lung Development ◽  
Surfactant Proteins ◽  
Nuclear Antigen ◽  
Lung Growth ◽  
Alveolar Cell ◽  
Epidermal Growth ◽  
Postnatal Lung Development ◽  
Proliferating Cell

We examined whether lung growth after pneumonectomy (PNX) invokes normal signaling pathways of postnatal development. We qualitatively and quantitatively assessed the immunoexpression of epidermal growth factor (EGF), its receptor (EGFR), surfactant proteins (SP) [SP-A and -D and surfactant proproteins (proSP)-B and -C] and proliferating cell nuclear antigen (PCNA) in immature and mature dog lung. We also assayed these proteins in lungs of immature dogs 3 wk or 10 mo after they underwent right PNX compared with simultaneous matched sham controls. During maturation, alveolar cell proliferation is regionally regulated in parallel with EGF and EGFR levels and inversely correlated with SP-A and proSP-C levels. In contrast, post-PNX lung growth is not associated with EGF or EGFR upregulation but with markedly increased SP-A level and moderately increased SP-D level; proSP-B and proSP-C levels did not change. We conclude that 1) signaling of EGF axis and differential regulation of SPs persist during postnatal lung development, 2) post-PNX lung growth is not a simple recapitulation of maturational responses, and 3) SP-A and SP-D may modulate post-PNX lung growth.

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.

scholarly journals Micron-sized intrapulmonary particle deposition in the developing rat lung

2012 ◽  
Vol 112 (5) ◽  
pp. 759-765
Author(s):  
Holger Schulz ◽  
Gunter Eder ◽  
Ines Bolle ◽  
Akira Tsuda ◽  
Stefan Karrasch
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Surface Area ◽  
Lung Development ◽  
Particle Deposition ◽  
Structural Changes ◽  
Breathing Patterns ◽  
Respiratory Parameters ◽  
Wistar Kyoto ◽  
Postnatal Lung Development

Little is known about the effects of postnatal developmental changes in lung architecture and breathing patterns on intrapulmonary particle deposition. We measured deposition in the developing Wistar-Kyoto rat, whose lung development largely parallels that of humans. Deposition of 2-μm sebacate particles was determined in anesthetized, intubated, spontaneously breathing rats on postnatal days (P) 7 to 90 by aerosol photometry (Karrasch S, Eder G, Bolle I, Tsuda A, Schulz H. J Appl Physiol 107: 1293–1299, 2009). Respiratory parameters were determined by body plethysmography. Tidal volume increased substantially from P7 (0.19 ml) to P90 (2.1 ml) while respiratory rate declined from 182 to 107/min. Breath-specific deposition was lowest (9%) at P7 and P90 and markedly higher at P35 (almost 16%). Structural changes of the alveolar region include a ninefold increase in surface area (Bolle I, Eder G, Takenaka S, Ganguly K, Karrasch S, Zeller C, Neuner M, Kreyling WG, Tsuda A, Schulz H. J Appl Physiol 104: 1167–1176, 2008). Particle deposition per unit of time and surface area peaked at P35 and showed a minimum at P90. At an inhaled particle number concentration of 105/cm3, there was an estimated 450, 690, and 330 particles/(min × cm2) at P7, P35, and P90, respectively. Multiple regression models showed that deposition depends on the mean linear intercept as structural component and the breathing parameters, tidal volume, and respiratory rate ( r2 > 0.9). In conclusion, micron-sized particle deposition was dependent on the stage of postnatal lung development. A maximum was observed during late alveolarization (P35), which corresponds to human lungs of about eight years of age. Children at this age may therefore be more susceptible to micron-sized airborne environmental health hazards.

scholarly journals Fetal and Neonatal Exposure to Nicotine Disrupts Postnatal Lung Development in Rats: Role of VEGF and Its Receptors

2011 ◽  
Vol 30 (2) ◽  
pp. 244-252 ◽  
Author(s):  
Maria A. Petre ◽  
Jim Petrik ◽  
Russ Ellis ◽  
Mark D. Inman ◽  
Alison C. Holloway ◽  
...  
Keyword(s):  
Lung Development ◽  
Female Rats ◽  
Neonatal Exposure ◽  
Nicotine Exposure ◽  
Smoking During Pregnancy ◽  
Vegf Signaling ◽  
Lung Structure ◽  
And Function ◽  
Postnatal Lung Development ◽  
Endothelial Growth Factor

Many women are unable to quit smoking during pregnancy and therefore are prescribed drugs, including nicotine (nicotine replacement therapy [NRT]), to aid with smoking cessation. However, the consequences to the offspring of pregnant NRT users have not been well studied. The goals of this study were to determine the consequences of fetal and neonatal exposure to nicotine on lung development and function. Female rats were exposed to nicotine for 2 weeks prior to mating until weaning. Lungs were collected from saline and nicotine-treated rats from birth to adulthood to assess postnatal lung structure and function. Although nicotine exposure altered alveolarization at weaning, an effect that resolved by adulthood, it did not affect lung function at any of the ages investigated. However, nicotine exposure significantly decreased lung vascularization. The current study suggests that perinatal exposure to nicotine alters lung development, an effect which may be mediated via decreased vascular endothelial growth factor (VEGF) signaling.

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