Proteomic analysis of a murine model of lung hypoplasia induced by oligohydramnios

Tanbir Najrana; Nagib  Ahsan; Rasha Abu-Eid; Alper Uzun; Lelia  Noble; George  Tollefson; Juan Sanchez-Esteban

doi:10.1002/ppul.25525

Proteomic analysis of a murine model of lung hypoplasia induced by oligohydramnios

Tanbir Najrana^* (Corresponding Author), Nagib Ahsan, Rasha Abu-Eid, Alper Uzun, Lelia Noble, George Tollefson, Juan Sanchez-Esteban

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

1 Citation (Scopus)

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.

Original language	English
Pages (from-to)	2740-2750
Number of pages	11
Journal	Pediatric Pulmonology
Volume	56
Issue number	8
Early online date	8 Jun 2021
DOIs	https://doi.org/10.1002/ppul.25525
Publication status	Published - 31 Aug 2021

Keywords

Lung
Mouse model
oligohydramnios
AKT1
SP-D

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Najrana_etal_PP_Proteomic_Analysis_Of_AAM
This is the peer reviewed version of the following article: Najrana T, Ahsan N, Abu‐Eid R, et al. Proteomic analysis of a murine model of lung hypoplasia induced by oligohydramnios. Pediatric Pulmonology. 2021;1‐11, which has been published in final form at http://doi.org/10.1002/ppul.25525. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.
Accepted author manuscript, 2.69 MBLicence: Unspecified

Cite this

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title = "Proteomic analysis of a murine model of lung hypoplasia induced by oligohydramnios",

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 underlyingmechanisms 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. LiquidChromatography-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 proteinscould play in fetal lung development. ",

keywords = "Lung, Mouse model, oligohydramnios, AKT1, SP-D",

author = "Tanbir Najrana and Nagib Ahsan and Rasha Abu-Eid and Alper Uzun and Lelia Noble and George Tollefson and Juan Sanchez-Esteban",

note = "Acknowledgments This 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",

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AU - Najrana, Tanbir

AU - Ahsan, Nagib

AU - Abu-Eid, Rasha

AU - Uzun, Alper

AU - Noble, Lelia

AU - Tollefson, George

AU - Sanchez-Esteban, Juan

N1 - Acknowledgments This 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

PY - 2021/8/31

Y1 - 2021/8/31

N2 - 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 underlyingmechanisms 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. LiquidChromatography-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 proteinscould play in fetal lung development.

AB - 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 underlyingmechanisms 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. LiquidChromatography-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 proteinscould play in fetal lung development.

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Proteomic analysis of a murine model of lung hypoplasia induced by oligohydramnios

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Keywords

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