The Genetics of Glucocorticoid-Regulated Embryonic Lung Morphogenesis
Year: 2000
Type: book-chapter
Abstract: Prenatal lung development is the result of complex interactions between epithelial and mesenchymal primordia, which require a relatively precise program of signal transduction and specific gene regulation. Elucidating the details of this program is important for understanding the etiology of pulmonary immaturity associated with respiratory distress syndrome (RDS), as well as for the development of effective preventive and treatment strategies. Lung morphogenesis has conclusively been shown to be under steroidal control (reviewed in refs. 1–30,see also Chapters 1–5, 7). Antenatal glucocorticoid (CORT) administration accelerates both morphogenesis and maturation (surfactant synthesis) of fetal lungs, reducing the incidence of neonatal RDS. Yet, in premature human births, significant racial, gender, and familial differences in the success of this steroid therapy are well known. Given the genetic susceptibility of infants to RDS (4,5), the observation of a maternal effect, the association between specific HLA haplotypes and glucocorticoid responsiveness (6), and the results of mouse studies (7–9), we postulated that the gene(s) at or near the major histocompatibility complex [(MHC), HLA in humans, H-2 in mice] may be related to the risk for developing RDS and the relative response to CORT treatment. The observation by Hafez and coworkers (10) of an association between specific HLA haplotypes and RDS supports this hypothesis.
Source: Humana Press eBooks
Authors: Tina Jaskoll, Michael Melnick
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
OpenAlex ID: W1354033