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 journalArticlepeer-review

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 languageEnglish
Pages (from-to)1-11
Number of pages11
JournalPediatric Pulmonology
Early online date8 Jun 2021
DOIs
Publication statusE-pub ahead of print - 8 Jun 2021

Keywords

  • Lung
  • Mouse model
  • oligohydramnios
  • AKT1
  • SP-D

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