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PubMed1995

Cell-specific expression of fibronectin in adult and developing rabbit lung.

Fibronectin (FN), a glycoprotein component of the extracellular matrix, plays a role in tissue morphogenesis and tissue-specific differentiation through its effects on cell adhesion, cell shape, and cytoskeletal organization. Immunohistochemistry has been used to show that during lung development FN deposition changes, yet the cell-specific sites of pulmonary FN synthesis have not been determined. Because cellular FN synthesis is reflected by FN mRNA abundance, we performed in situ hybridizations to identify pulmonary tissue with the capacity to synthesize FN. Both in situ mRNA hybridization and immunohistochemical staining were performed on tissue sections from lungs of adults and late gestation fetal and neonatal rabbits. In adults, FN transcripts and immunostaining were clearly seen in endothelial cells, smooth muscle cells, and chondrocytes. During lung development, FN transcripts were virtually ubiquitous except in airway epithelium. There was a gradual decrease in FN mRNA abundance with advancing fetal age, but low levels of FN mRNA persisted in neonatal and adult lungs. In contrast, parenchymal immunostaining increased throughout fetal development and remained elevated in the newborn. FN immunostaining was lower in adult lung. In all tissues examined, airway epithelial cells contained no FN transcripts above background. However, immunostaining was detected in airway basement membrane zones and on luminal surfaces of some epithelial cells. The lack of FN transcripts in airway epithelial cells suggests that FN synthesis does not normally occur in this cell type and that its associated FN immunostaining is from another source. The colocalization of FN mRNA and protein in pulmonary endothelial cells, smooth muscle cells, and chondrocytes in adults strongly suggests that these cells are sites of FN synthesis.

Animals↗
PubMed1989

Ultrastructural and biochemical evidence of glycogen in the developing lung of the chick embryo: possible contribution to surfactant.

1. Glycogen was identified ultrastructurally in undifferentiated type-II cells of the lung of the day 16 chick embryo. 2. By 4 days after hatching, glycogen in type-II cells could not be observed, although lungs were actively secreting surfactant. 3. Biochemical measurements of pulmonary glycogen revealed a depletion during days 14-20 of incubation, corroborating ultrastructural data. 4. Using lung slices, 14C-glucose was incorporated in vitro into pulmonary surfactant phospholipids at a high rate in day 14 embryos, and a significantly lower rate on day 19. 5. Hypophysectomy resulted in sub-normal initial accumulation of pulmonary glycogen on day 14 of development, but did not alter the depletion pattern after day 16. 6. Thus, glycogen stores may contribute to avian embryonic pulmonary surfactant, and accumulation of early stores may be under hormonal control.

Animals↗
PubMed1995

Abnormal lung development and cleft palate in mice lacking TGF-beta 3 indicates defects of epithelial-mesenchymal interaction.

A broad spectrum of biological activities has been proposed for transforming growth factor-beta 3 (TGF-beta 3). To study TGF-beta 3 function in development, TGF-beta 3 null mutant mice were generated by gene-targeting. Within 20 hours of birth, homozygous TGF-beta 3-/- mice die with unique and consistent phenotypic features including delayed pulmonary development and defective palatogenesis. Unlike other null mutants with cleft palate, TGF-beta 3-/- mice lack other concomitant craniofacial abnormalities. This study demonstrates an essential function for TGF-beta 3 in the normal morphogenesis of palate and lung, and directly implicates this cytokine in mechanisms of epithelial-mesenchymal interaction.

Animals↗
PubMed1984

Functional changes in the regulatory subunit of the type II cyclic adenosine 3':5'-monophosphate-dependent protein kinase isozyme during normal and neoplastic lung development.

The abilities of cyclic adenosine 3':5'-monophosphate (cAMP) and cyclic 8-azidoadenosine 3':5'-[32P]monophosphate (8-N3-[32P]cAMP) to bind to the regulatory subunit (RII) of the type II cAMP-dependent protein kinase isozyme and to cause subsequent dissociation of the holoenzyme were compared in extracts from adult and neonatal mouse lung and lung adenoma. RII in extracts from adult lung exhibits equal numbers of high- (Kd 15 nM) and low- (Kd 230 nM) affinity 8-N3-[32P]cAMP binding sites. In the neonate, the proportion of high-affinity sites is reduced to 20% while, in lung adenoma, only low-affinity RII binding is observed. Low-affinity RII binding is correlated with an inability of cAMP to dissociate the type II holoenzyme completely. Sucrose gradient sedimentation of adult lung cytosol in the presence of cAMP shows complete dissociation of the type I isozyme, while only some of the type II holoenzyme is dissociated. This is in contrast to the case with lung tumor cytosol, in which only low-affinity binding is observed and no apparent dissociation of the type II isozyme occurs. cAMP does promote RII dephosphorylation within the holoenzyme, however, suggesting that cAMP can bind to RII without dissociating the tetramer. Consistent with this interpretation, photoincorporation of 8-N3-[32P]cAMP prior to sucrose gradient sedimentation results in the formation of a photolabeled RII complex which sediments at the same rate as does the holoenzyme. Two-dimensional gel electrophoresis of RII photolabeled at low and high concentrations of 8-N3-[32P]cAMP suggests that these altered binding and dissociation characteristics of the type II isozyme are not due to the presence of a structurally altered RII molecule. After DEAE-cellulose chromatography of lung cytosol, only high-affinity RII binding is observed, and all of the RII can now be dissociated with cAMP. Low-affinity binding may thus reflect either an altered conformational state of RII or the interaction of the type II kinase with other cytosolic molecules which can affect RII binding and dissociation without altering the functional properties of the type I isozyme.

Adenoma↗
PubMed1978

Angiotensin-converting enzyme in developing lung and kidney.

Angiontensin-converting enzyme (ACE) catalyzes rapid conversion of angiotensin II (AII). This enzyme has been identified in the vascular endothelium of nearly every tissue. Inasmuch as AII is the biologically active component of the renin-angiotensin system, and since age-related differences exist in the renin-angiotensin system, it was of interest to determine converting enzyme activity during development. ACE activity was quantified by measuring the optical density of hippuric acid liberated from hippuryl-L-histidyl-L-leucine (HHL) following incubation with the 20,000 X g supernatant of tissue homogenates. Pulmonary ACE activity of near-term fetal rats was not different than 1-day-old animals. Therafter, ACE activity increased during the first 6 wk postpartum in a biphasic manner. A similar age-dependent increase in converting enzyme activity was observed in rat kidney, mouse kidney, and mouse lung. Substrate affinity of all enzymes measured was similar, suggesting that the age-related increase in activity was due to increased enzyme content. The low activity of ACE in the newborn might function to limit AII production.

Aging↗
PubMed1989

Cytodifferentiation of two epithelial populations of the respiratory bronchiole during fetal lung development in the rhesus monkey.

This study describes the cytodifferentiation of the two populations of epithelial cells found in the respiratory bronchiole of the adult rhesus monkey. One population, pseudostratified and containing ciliated, nonciliated secretory, and basal cells, is found overlying the pulmonary artery (PA). The other population, not associated with the PA, contains nonciliated cuboidal cells between alveolar outpockets. In this study we used terminal conducting airways from the lungs of fetal (90 to 155 days gestational age [DGA]), postnatal, and adult rhesus monkeys. Ciliated cells were partially differentiated at 90 DGA (54% gestation) and completely differentiated by 134 DGA (80% gestation). Nonciliated secretory cells were partially differentiated at 95 DGA (57% gestation) but did not lose all glycogen until the postnatal period. Basal cells appeared by 134 DGA (80% gestation) and matured in the postnatal period. Small mucous granule cells appeared at 125 DGA (74% gestation) and did not change throughout fetal development. Neuroendocrine cells were present throughout the entire period studied. Nonciliated cuboidal bronchiolar cells of the nonciliated population of the respiratory bronchiole appeared at 105 DGA (62% gestation) and matured in the postnatal period. We conclude that 1) although most of the differentiation of the lower airway occurs before birth, most of the cell types are not completely differentiated at birth; 2) the sequence of differentiation for the cells of the ciliated pseudostratified epithelial population is ciliated, nonciliated secretory, and basal; 3) the sequence of differentiation for the nonciliated secretory cell is similar to that of the secretory cells in more proximal airways; and 4) basal, neuroendocrine, and small mucous granule cells are not a part of the differentiation sequence of the other cell types.

Animals↗
PubMed2000

Lung development following diaphragmatic hernia in the fetal rabbit.

Diaphragmatic hernia was created in 39 rabbit fetuses on day 23 of gestation. Fifteen fetuses underwent a sham thoracotomy (SHAM). Thirty-nine non-operated littermates served as internal controls (CTR). Fetuses were harvested by Caesarean section on days 25, 27, 29 and 30 of gestation. Pulmonary response was evaluated by lung to body weight ratio (LBWR), morphometry, and density of type II pneumocytes. No difference was found between CTR and SHAM fetuses at term. CDH fetuses had smaller lungs (LBWR 0.014 +/- 0.004 versus 0.030 +/- 0.04 in CTR, P < 0.0001), a less complex acinus [mean terminal bronchial density (MTBD) 1.786 +/- 0.408 versus 0.917 +/- 0. 188, P < 0.0001], thicker alveolar septa [mean wall transection length (LMW) 0.0221 +/- 0.008 versus 0.0142 +/- 0.002, P = 0.0003], and a lower type II cell count (144.5 +/- 19.33 versus 216.2 +/- 27.85 per high power field, P < 0.0001). The differences in MTBD and LMW were significant from gestational day 25 onwards, and the differences in type II cell count from day 27 onwards. Surgical diaphragmatic hernia in rabbit fetuses in the late pseudoglandular phase reproduces many features of the pulmonary hypoplasia associated with human congenital diaphragmatic hernia, including the delayed maturation. The effects are present within 2 days following experimental diaphragmatic hernia and progress over time.

Animals↗
PubMed1987

Fetal breathing movements are not a reliable predictor of continued lung development in pregnancies complicated by oligohydramnios.

Fetal breathing activity was monitored by ultrasonography in 14 patients with oligohydramnios (4 with fetal anuria and 10 with premature rupture of the membranes). 45 patients with intact membranes, with normal amniotic fluid volume, and matched for gestational age were the controls. Fetal breathing movements were seen in all 8 patients who died in the perinatal period with a necropsy diagnosis of lung hypoplasia. While patients with premature rupture of the membranes (irrespective of outcome) spent the same or less time breathing than controls, fetuses with renal anomalies, oligohydramnios, and lung hypoplasia spent more time breathing than controls. The observation of fetal breathing activity is not helpful in identifying patients with oligohydramnios at risk of lung hypoplasia.

Amniotic Fluid↗
PubMed1984

The role of lung development in the age-related susceptibility of ferrets to influenza virus.

Newborn (I-day-old) ferrets died following intranasal inoculation of influenza virus (clone 7a) but suckling (15-day-old) ferrets were almost as resistant as adult ferrets. Many of the deaths in newborn ferrets were consequent upon an increased lower respiratory tract infection. One reason for the latter was an increase in susceptibility of both ciliated epithelium and alveolar cells in newborn ferret lungs when compared with the corresponding cells in adult and suckling ferrets (Coates et al. 1984). Work reported here shows that the lungs of newborn ferrets possess a greater proportion of ciliated epithelium-lined airway in comparison with the lungs of suckling and adult ferrets. This situation might also contribute to the increased susceptibility of the lower respiratory tract although the difficulties of assessing this influence precisely are discussed. In addition, the occlusion of the narrower airways of the immature lung in the infected newborn ferret contributes to the increased respiratory complications.

Age Factors↗