Amniotic fluid inflammation and fetal lung development

2006 ◽  
pp. 173-186
Author(s):  
Timothy Moss ◽  
Alan Jobe
Keyword(s):  
Amniotic Fluid ◽  
Lung Development ◽  
Fetal Lung ◽  
Fetal Lung Development

scholarly journals Amniotic Fluid Lecithin: Sphingomyelin Ratio and Fetal Lung Development

BMJ ◽  
1972 ◽  
Vol 2 (5805) ◽  
pp. 85-86 ◽  
Author(s):  
C. R. Whitfield ◽  
W. H. Chan ◽  
W. B. Sproule ◽  
A. D. Stewart
Keyword(s):  
Amniotic Fluid ◽  
Lung Development ◽  
Fetal Lung ◽  
Fetal Lung Development

scholarly journals Impaired Fetal Lung Development can be Rescued by Administration of Extracellular Vesicles Derived from Amniotic Fluid Stem Cells

2020 ◽  
Author(s):  
Lina Antounians ◽  
Vincenzo D. Catania ◽  
Louise Montalva ◽  
Benjamin D. Liu ◽  
Huayun Hou ◽  
...  
Keyword(s):  
Stem Cells ◽  
Amniotic Fluid ◽  
Extracellular Vesicles ◽  
Lung Development ◽  
Pulmonary Hypoplasia ◽  
Fetal Lung ◽  
Branching Morphogenesis ◽  
Amniotic Fluid Stem Cells ◽  
Fetal Lung Development ◽  
Regenerative Ability

AbstractIncomplete lung development, also known as pulmonary hypoplasia, is a recognized cause of neonatal death and poor outcome for survivors. To date, there is no effective treatment that promotes fetal lung growth and maturation. Herein, we describe a novel stem cell-based approach that enhances fetal lung development via the administration of extracellular vesicles (EVs) derived from amniotic fluid stem cells (AFSCs). In experimental models of pulmonary hypoplasia, administration of AFSC-EVs promoted lung branching morphogenesis and alveolarization, and stimulated pulmonary epithelial cell and fibroblast differentiation. This regenerative ability was confirmed in two models of injured human lung cells, where human AFSC-EVs obtained following good manufacturing practices restored pulmonary epithelial homeostasis. AFSC-EV beneficial effects were exerted via the release of RNA cargo, primarily miRNAs, that regulate the expression of genes involved in fetal lung development. Our findings suggest that AFSC-EVs hold regenerative ability for underdeveloped fetal lungs, demonstrating potential for therapeutic application.One Sentence SummaryFetal lung regeneration via administration of extracellular vesicles derived from amniotic fluid stem cells

Fetal lung development via quantitative biomarkers from diffusion MRI and histological validation in rhesus macaques

2021 ◽  
Author(s):  
Nara S. Higano ◽  
Xuefeng Cao ◽  
Jinbang Guo ◽  
Xiaojie Wang ◽  
Christopher D. Kroenke ◽  
...  
Keyword(s):  
Lung Development ◽  
Diffusion Mri ◽  
Rhesus Macaques ◽  
Fetal Lung ◽  
Fetal Lung Development ◽  
Histological Validation

scholarly journals Amniotic fluid stem cell extracellular vesicles promote fetal lung branching and cell differentiation in experimental congenital diaphragmatic hernia

2022 ◽  
Author(s):  
Kasra Khalaj ◽  
Rebeca Lopes Figueira ◽  
Lina Antounians ◽  
Sree Gandhi ◽  
Matthew Wales ◽  
...  
Keyword(s):  
Amniotic Fluid ◽  
Congenital Diaphragmatic Hernia ◽  
Extracellular Vesicles ◽  
Diaphragmatic Hernia ◽  
Lung Development ◽  
Pulmonary Hypoplasia ◽  
Fetal Lung ◽  
Branching Morphogenesis ◽  
Neuroendocrine Cells ◽  
Beta Catenin

Pulmonary hypoplasia secondary to congenital diaphragmatic hernia (CDH) is characterized by impaired branching morphogenesis and differentiation. We have previously demonstrated that administration of extracellular vesicles derived from rat amniotic fluid stem cells (AFSC-EVs) rescues development of hypoplastic lungs at the pseudoglandular and alveolar stages in rodent models of CDH. Herein, we tested whether AFSC-EVs exert their regenerative effects at the canalicular and saccular stages, as these are translationally relevant for clinical intervention. To induce fetal pulmonary hypoplasia, we gavaged rat dams with nitrofen at embryonic day 9.5 and demonstrated that nitrofen-exposed lungs had impaired branching morphogenesis, dysregulated signaling pathways relevant to lung development (FGF10/FGFR2, ROBO/SLIT, Ephrin, Neuropilin 1, beta-catenin) and impaired epithelial and mesenchymal cell marker expression at both stages. AFSC-EVs administered to nitrofen-exposed lung explants rescued airspace density and increased the expression levels of key factors responsible for branching morphogenesis. Moreover, AFSC-EVs rescued the expression of alveolar type 1 and 2 cell markers at both canalicular and saccular stages, and restored markers of club, ciliated epithelial, and pulmonary neuroendocrine cells at the saccular stage. AFSC-EV treated lungs also had restored markers of lipofibroblasts and PDGFRA+ cells to control levels at both stages. EV tracking showed uptake of AFSC-EV RNA cargo throughout the fetal lung and an mRNA-miRNA network analysis identified that several miRNAs responsible for regulating lung development processes were contained in the AFSC-EV cargo. These findings suggest that AFSC-EV based therapies hold potential for restoring fetal lung growth and maturation in babies with pulmonary hypoplasia secondary to CDH.

scholarly journals In utero administration of GABA promotes fetal lung development

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Narendranath Reddy Chintagari ◽  
Yang Wang ◽  
Dong Xi ◽  
Lin Liu
Keyword(s):  
Lung Development ◽  
Fetal Lung ◽  
In Utero ◽  
Fetal Lung Development

scholarly journals MicroRNA-127 modulates fetal lung development

2009 ◽  
Vol 37 (3) ◽  
pp. 268-278 ◽  
Author(s):  
Manoj Bhaskaran ◽  
Yang Wang ◽  
Honghao Zhang ◽  
Tingting Weng ◽  
Pradyumna Baviskar ◽  
...  
Keyword(s):  
Expression Pattern ◽  
Lung Development ◽  
Fetal Lung ◽  
Mirna Microarray ◽  
Mirna Expression Pattern ◽  
Opposite Trend ◽  
Fetal Lung Development ◽  
Terminal Bud ◽  
Lung Organ Culture

MicroRNAs (miRNAs) are small endogenous RNAs and are widely regarded as one of the most important regulators of gene expression in both plants and animals. To define the roles of miRNAs in fetal lung development, we profiled the miRNA expression pattern during lung development with a miRNA microarray. We identified 21 miRNAs that showed significant changes in expression during lung development. These miRNAs were grouped into four distinct clusters based on their expression pattern. Cluster 1 contained miRNAs whose expression increased as development progressed, while clusters 2 and 3 showed the opposite trend of expression. miRNAs in cluster 4 including miRNA-127 (miR-127) had the highest expression at the late stage of fetal lung development. Quantitative real-time PCR validated the microarray results of six selected miRNAs. In situ hybridization demonstrated that miR-127 expression gradually shifted from mesenchymal cells to epithelial cells as development progressed. Overexpression of miR-127 in fetal lung organ culture significantly decreased the terminal bud count, increased terminal and internal bud sizes, and caused unevenness in bud sizes, indicating improper development. These findings suggest that miR-127 may have an important role in fetal lung development.

Sign in / Sign up

Export Citation Format

Share Document