Tanbir Najrana1, Lauren M Ramos1, Rasha Abu Eid2, Juan Sanchez-Esteban1. 1. Department of Pediatrics, Alpert Medical School of Brown University, Women & Infants Hospital of Rhode Island, 101 Dudley Street, Providence 02905, Rhode Island. 2. Dental School, University of Aberdeen, Aberdeen, Scotland, United Kingdom.
Abstract
BACKGROUND AND OBJECTIVE: Severe oligohydramnios can induce pulmonary hypoplasia. However, the mechanisms by which leaking of fluids cause lung hypoplasia are not well defined. The objective of this study was to characterize a mouse model of pulmonary hypoplasia induced by oligohydramnios. METHODS: Amniotic sacs were punctured on E14.5 of gestation. Untouched fetuses were used as control. Pregnancy was allowed to continue until E18.5 in which lung tissue was collected and evaluated for morphometry, proliferation, differentiation, apoptosis, and angiogenesis. RESULTS: Our results found that lung weight, lung to total body weight ratio, and lung water content were reduced in oligohydramnios when compared to controls. In contrast, oligohydramnios did not affect the DNA content. Morphometric studies confirmed that oligohydramnios fetuses had smaller air spaces than control. Interestingly, cells from oligohydramnios fetuses have smaller size and less regular shapes. Oligohydramnios decreased the differentiation of type I epithelial cells and compromised apoptosis and angiogenesis while proliferation was not affected. CONCLUSIONS: Although, the smaller size of the lung could be explained by a decreased of lung fluids, our data suggest that increased of external compression secondary to severe oligohydramnios can compromise cell size and interfere with epithelial and endothelial development. Type I epithelial cells could have an unrecognized key role in the differentiation of the distal lung mediated by mechanical signals. Pediatr Pulmonol. 2017;52:746-756.
BACKGROUND AND OBJECTIVE: Severe oligohydramnios can induce pulmonary hypoplasia. However, the mechanisms by which leaking of fluids cause lung hypoplasia are not well defined. The objective of this study was to characterize a mouse model of pulmonary hypoplasia induced by oligohydramnios. METHODS: Amniotic sacs were punctured on E14.5 of gestation. Untouched fetuses were used as control. Pregnancy was allowed to continue until E18.5 in which lung tissue was collected and evaluated for morphometry, proliferation, differentiation, apoptosis, and angiogenesis. RESULTS: Our results found that lung weight, lung to total body weight ratio, and lung water content were reduced in oligohydramnios when compared to controls. In contrast, oligohydramnios did not affect the DNA content. Morphometric studies confirmed that oligohydramnios fetuses had smaller air spaces than control. Interestingly, cells from oligohydramnios fetuses have smaller size and less regular shapes. Oligohydramnios decreased the differentiation of type I epithelial cells and compromised apoptosis and angiogenesis while proliferation was not affected. CONCLUSIONS: Although, the smaller size of the lung could be explained by a decreased of lung fluids, our data suggest that increased of external compression secondary to severe oligohydramnios can compromise cell size and interfere with epithelial and endothelial development. Type I epithelial cells could have an unrecognized key role in the differentiation of the distal lung mediated by mechanical signals. Pediatr Pulmonol. 2017;52:746-756.
Authors: Tanbir Najrana; Anshu Mahadeo; Rasha Abu-Eid; Elena Kreienberg; Victoria Schulte; Alper Uzun; Christoph Schorl; Laura Goldberg; Peter Quesenberry; Juan Sanchez-Esteban Journal: J Cell Physiol Date: 2020-01-22 Impact factor: 6.384
Authors: Philipp Foessleitner; Konrad Hoetzenecker; Alberto Benazzo; Katrin Klebermass-Schrehof; Anke Scharrer; Herbert Kiss; Alex Farr Journal: Am J Transplant Date: 2021-08-09 Impact factor: 9.369