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PubMed2003

Fetal lung development in the elephant reflects the adaptations required for snorkeling in adult life.

The adult elephant is unique among mammals in that the pleural membranes are thickened and the pleural cavity is obliterated by connective tissue. It has been suggested that this peculiar anatomy developed because the animal can snorkel at depth, and this behavior subjects the microvessels in the parietal pleura to a very large transmural pressure. To investigate the development of the parietal pleura, the thickness of the endothoracic fascia (ET) was measured in four fetal African elephants of approximate gestational age 111-130 days, and the appearances were compared with those in human, rabbit, rat and mouse fetuses of approximately the same stage of lung organogenesis. The mean thicknesses of ET in the elephant, human, rabbit, rat and mouse were 403, 53, 29, 27 and 37 microm, respectively. This very early development of a thick parietal pleura in the elephant fetus is consistent with the hypothesis of a long history of snorkeling in the elephant's putative aquatic ancestors.

Adaptation, Biological↗
PubMed1992

Expression of fibronectin, the integrin alpha 5, and alpha-smooth muscle actin in heart and lung development.

The developmentally regulated expression of fibronectin (FN) in developing organs and FN's ability to stimulate cell migration and differentiation in vitro suggest a role in organogenesis. We examined the distribution of FN and the alpha 5 subunit of its receptor, the integrin alpha 5 beta 1, in the lungs and hearts of murine embryos at 11, 13, 16, and 18 days of gestation. In the lung, FN staining was present in the mesenchyme and parabronchial cells at day 11, increased at day 13, and decreased after day 16. Increases in FN coincided with the period of branching morphogenesis, and FN was concentrated at areas of airway bifurcation, suggesting a role for FN in cleft formation. The alpha 5 subunit appeared later at 13 days, co-distributing with FN only in well-developed primary bronchioles. At all stages, alpha-smooth muscle actin expression correlated temporally and spatially with that of the alpha 5 subunit. In the heart, staining for FN, the alpha 5 subunit, and alpha-smooth muscle actin were present at day 11 and increased at day 13. FN was present in the outflow tract and developing atria and ventricles, where it was concentrated in the outer layer or visceral pericardium. Interestingly, alpha 5 was detected at the inner layer, the endothelium, lining the outflow tract and atrioventricular cushions where endothelial cells migrate into the cardiac jelly in the process of epithelial-mesenchymal transformation. This suggests a potential role for alpha 5 beta 1 and FN in ventricular septation and valve formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1996

Expression of gastrin-releasing peptide receptor gene in developing lung.

Bombesin (BN) or its mammalian counterpart, Gastrin-releasing peptide (GRP) is produced by pulmonary neuroendocrine cells (PNEC). The function of GRP as a growth factor involves lung morphogenesis, but the precise mechanism and the target cells have not been defined. We used a nonradioactive in situ hybridization (NISH) and Northern blot analysis for both GRP receptor (GRP-R) and its ligand GRP on samples of fetal and newborn human and rabbit lung. For immunolocalization of BN/GRP and the proliferating lung cell population we used anti-BN/GRP or MIB-1 antibodies, respectively. NISH and Northern blot showed peak expression of GRP-R mRNA on day 24 gestation in the fetal rabbit lung. At the cellular level, GRP-R mRNA was localized mainly in the distal airway epithelial tubes and surrounding mesenchyme, whereas proximal airways showed decreased signal. Epithelium expressing GRP-R showed positive labeling for proliferation antigen in contrast to PNEC, which were negative. In human post-natal lung, strong signal for GRP-R mRNA was localized in the airway epithelial cells and submucosal glands. PNEC in both rabbit and human lung expressed mRNA for GRP, but only in human lung were they immunoreactive for the peptide. However BN/GRP immunoreactive cells were detected in rabbit fetal lung culture. The expression of GRP-R in mammalian lung is developmentally regulated, peaking both spatially and temporally during the phase of rapid airway growth and differentiation. Both epithelial and mesenchymal components express GRP-R consistent with paracrine mechanism for GRP activity during lung morphogenesis.

3T3 Cells↗
PubMed2000

From fruitflies to mammals: mechanisms of signalling via the Sonic hedgehog pathway in lung development.

The hedgehog signalling pathway has been implicated in many different processes in fly and vertebrate development. It is now known that the hedgehog cascade is crucial for the patterning of the early respiratory system. Hedgehog signalling in the lung involves Gli transcription proteins, but their potential downstream target genes have yet to be identified. Bmp4 and Fgf10 have been shown to regulate lung branching morphogenesis but seem not to be targets of hedgehog signalling.

Animals↗
PubMed1987

Interaction of prenatal starvation and dexamethasone treatment on lung development in newborn guinea pigs.

Prenatal starvation causes pulmonary hypoplasia, retarded alveolarization, and reduced surfactant production in newborn guinea pigs. This study examined the potential benefit of simultaneous transplacental dexamethasone, which accelerates fetal lung maturation in other species. Pregnant guinea pigs were placed in 1 of 4 groups: Control (C), fed ad libitum until term (67 days) and given daily saline injections from Day 55 of gestation until term; Dexamethasone (D), fed as Group C but given daily injections of 2.0 mg dexamethasone/kg BW from Day 55 until term; Starved (S), given 50% rations from Day 45 until term and injected as Group C; Starved + Dexamethasone (SD), fed as Group S and injected as Group D. Controls and Group D did not differ in body or lung weight, DNA, protein, or lung volume (VL), but Group D lungs contained more lavageable and tissue surfactant, total alveolar surface area (Sa), and membrane diffusing capacity (DmO2) because of increased alveolar surface density. The S neonates weighed 38% less than controls, with proportional reductions in lung weight, DNA, protein, lavage and tissue phospholipids, VL, Sa septal tissue, capillary surface area (Sc), and DmO2. Compared with these S neonates, the SD neonates did not differ for BW, lung weight, DNA, protein, phospholipids, or VL, but their lungs contained significantly more Sa, Sc, epithelial and endothelial tissue volumes, and a higher alveolar surface density. These differences resulted in an average DmO2 for SD neonates that was indistinguishable from that of controls, and correlated with greater viability among the smallest SD animals compared with those in Group S.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

Lung development in the fetal primate Macaca nemestrina. III. HMD.

Delivery of M. nemestrina at 80% of normal gestation provides a population of neonates at high risk for hyaline membrane disease (HMD). The diagnosis of HMD was made by the presence of reticulogranular densities and air bronchograms on chest radiographs. Patchy atelectasis was seen in the lungs of animals assigned by clinical and radiographic criteria to the HMD group and not in the normal lungs of animals matched for gestational and postnatal age. Total phospholipid and phosphatidylcholine in whole lung, airway lavage fluid, and surface-active materials were lower in animals with HMD. Amniotic fluid L/S ratios were lower in the group that developed HMD. Pressure-volume measurements indicated decreased distensibility and unstable terminal air spaces in the HMD group. Alveolar-arterial oxygen pressure differences were greater in animals with HMD. There were no differences between HMD and normal groups in body weight, lung weight, percent dry lung weight, gestational age, and postnatal age at death. This primate species, subjected to premature delivery, is a suitable animal model of HMD in human neonates.

Amniotic Fluid↗