Ontogeny of embryonic chicken lung: Effects of pituitary gland, corticosterone, and other hormones upon pulmonary growth and synthesis of surfactant phospholipids

Abstract

The actions of hormones on growth, cellular proliferation, and on synthetic rates of the major surfactant phospholipids, phosphatidylcholine (PC) and disaturated PC (DSPC), were studied in the lung of the chick embryo. Particular emphasis was placed on the effects of hypophysectomy, pituitary transplantation, and treatment with corticosterone (CORT). One study was concerned with hydrocortisone (HYCORT), estrogen (E2), thyroxine (T4), ovine prolactin (oPRL), and insulin. Hypophysectomy interfered with the normal gain in protein, the progressive dehydration of the embryonic lung, and also caused a reduction in the number of pulmonary cells on Days 16 and 18 of incubation. Absence of the pituitary gland diminished pulmonary PC by Day 16. Transplantation of one pituitary gland or exogenous CORT partially restored pulmonary phospholipid and PC (normalized per wet weight) in hypophysectomized (hypox) embryos. Transplantation also restored relative protein content in lungs of hypox individuals. Beyond this, transplantation was generally ineffective in reversing deficits of hypox individuals. All concentrations of CORT administered (30-100-300 micrograms) reduced the rate of pulmonary cell division. The highest dose was toxic as judged by its capacity to cause cellular death. Treatment of intact chicken embryos with CORT or E2 for two days stimulated incorporation of [14C]choline into PC and DSPC (the most surface-active component of PC) in the lungs of Day 17 embryos. CORT, but not E2, stimulated DSPC synthesis when treatment was increased to 3 days. Other hormones tested (T4, oPRL, insulin, and HYCORT) had no effect upon the rate of incorporation of [14C]choline into PC or DSPC. These results indicate that during ontogeny the avian lung becomes sensitive to CORT, and possibly E2, prior to 16 days of incubation. CORT, in particular, acts both to trigger the prehatching stimulation of surfactant phospholipid synthesis, especially the vital DSPC fraction, and to slow the rate of pulmonary cellular division coincident with biochemical differentiation of the surfactant system.

Pulmonary Vascular Endothelial Growth Factor Expression and Disaturated Phospholipid Content in a Chicken Model of Hypoxia-Induced Fetal Growth Restriction

“…On the other hand, important similarities are present, such as the stimulatory effect of corticosteroids on surfactant production [22,41] . Regarding the role of growth factors in the regulation of avian lung development, there is an important lack of data, as stressed by Maina [34] .…”

“…The molecular mechanisms that regulate lung development differ to some extent between species, including humans and chickens [38,41] . On the other hand, important similarities are present, such as the stimulatory effect of corticosteroids on surfactant production [22,41] .…”

Cracking the Egg: Potential of the Developing Chicken as a Model System for Nonclinical Safety Studies of Pharmaceuticals

“…Neuronal growth and plasticity (Johnson and Jope, 1992) NeuN Marker for neuronal maturation (Sarnat et al, 1998) S-100 Marker enabling monitoring of brain injury in blood and CSF (Sun et al, 2012 Surfactants increase compliance, lower surface tension, and prevent atelectasis of the lungs; lack of surfactants causes respiratory distress of the newborn Hylka and Doneen, 1983;Makanya et al, 2007Makanya et al, , 2013Been et al, 2010;Bjornstad et al, 2014 Aquaporin 5 Expressed in human type I pneumocytes, vital for gas exchange (Kreda et al, 2001) Caveolin 1…”

“…This is still a highly relevant clinical problem, and experimental embryo animal model systems in which the effects of different corticosteroids on lung development can be monitored are crucial. Hylka and Doneen (1983) used the chicken embryo model to study the actions of steroid hormones on the fetal lung. This study used growth, cellular proliferation, and rate of synthesis of the major surfactant phospholipids as parameters of lung development and function.…”

“…This study used growth, cellular proliferation, and rate of synthesis of the major surfactant phospholipids as parameters of lung development and function. Further, effects on lung development of in ovo hypophysectomy and treatment with corticosterone or pituitary transplantation were assessed (Hylka and Doneen, 1983). Antenatal corticosteroid treatment is also associated with impaired cerebellar development in humans, a finding that has been reproduced in the chicken embryo (Aden et al, 2008(Aden et al, , 2011.…”