Abstract
Severe oligohydramnios (OH) due to prolonged loss of amniotic fluid can cause pulmonary hypoplasia. Animal model of pulmonary hypoplasia induced by amniotic fluid drainage is partly attributed to changes in mechanical compression of the lung. Although numerous studies on OHmodel have demonstrated changes in several individual proteins, however the underlying
mechanisms for interrupting normal lung development in response to decrease of amniotic fluid volume is not fully understood. In this study, we used a proteomic approach to explore differences in the expression of a wide-range of proteins after induction of OH in a mouse model of pulmonary hypoplasia to find out the signaling/molecular pathways involve in fetal lung development. Liquid
Chromatography-MassSpectromery/MassSpectrometry (LC-MS/MS) analysis found 474 proteins that were differentially expressed in OH induced hypoplastic lungs in comparison to untouched (UnT) control. Among these proteins, we confirmed the downregulation of AKT1, SP-D and CD200, and provided proof-of-concept for the first time about the potential role that these proteins
could play in fetal lung development.
mechanisms for interrupting normal lung development in response to decrease of amniotic fluid volume is not fully understood. In this study, we used a proteomic approach to explore differences in the expression of a wide-range of proteins after induction of OH in a mouse model of pulmonary hypoplasia to find out the signaling/molecular pathways involve in fetal lung development. Liquid
Chromatography-MassSpectromery/MassSpectrometry (LC-MS/MS) analysis found 474 proteins that were differentially expressed in OH induced hypoplastic lungs in comparison to untouched (UnT) control. Among these proteins, we confirmed the downregulation of AKT1, SP-D and CD200, and provided proof-of-concept for the first time about the potential role that these proteins
could play in fetal lung development.
Original language | English |
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Pages (from-to) | 2740-2750 |
Number of pages | 11 |
Journal | Pediatric Pulmonology |
Volume | 56 |
Issue number | 8 |
Early online date | 8 Jun 2021 |
DOIs | |
Publication status | Published - 31 Aug 2021 |
Bibliographical note
AcknowledgmentsThis work was supported by funding from the National Institute of General Medical Sciences of the National Institutes of Health, Number: P30GM114750 and Oh–Zopfi Grant for Perinatal Research, Department of Pediatrics; Kilguss Research Core at Women & Infants Hospital of Rhode Island.
Funding information
National Institute of General Medical Sciences, Grant/Award Number: 30GM114750; Oh–Zopfi Award for Perinatal Research, Women & Infants Hospital of Rhode Island
Keywords
- Lung
- Mouse model
- oligohydramnios
- AKT1
- SP-D