Poster Session 3
Category: Fetal Intervention
Poster Session 3
Nilhan Torlak, PhD
Postdoctoral Fellow
New York University Langone Health Fetal Research Lab
New York, New York, United States
Fernando Ferrer-Marquez, MD, PhD
Center for Fetal and Placental Research, Cincinnati Children’s Hospital Medical Center
Cincinnati, Ohio, United States
Josephine Kemp
Center for Fetal and Placental Research, Cincinnati Children’s Hospital Medical Center
Cincinnati, Ohio, United States
Marc Oria, PhD
Center for Fetal and Placental Research, Cincinnati Children’s Hospital Medical Center
Cincinnati, Ohio, United States
Marco Klein
Sciomics
Heidelberg, Baden-Wurttemberg, Germany
Ronny Schmidt, PhD
Sciomics
Heidelberg, Baden-Wurttemberg, Germany
Christoph Schroeder, PhD
Sciomics
Heidelberg, Baden-Wurttemberg, Germany
Braxton Forde, MD
Assistant Professor
Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, College of Medicine, University of Cincinnati
Cincinnati, Ohio, United States
Emrah Aydin, MBA, MD, PhD
Center for Fetal and Placental Research, Cincinnati Children’s Hospital Medical Center
Cincinnati, Ohio, United States
Jose L. Peiro, MD, PhD
New York University Langone Health Fetal Research Lab
New York, New York, United States
Congenital diaphragmatic hernia (CDH) leads to pulmonary hypoplasia, hypertension, and abnormal placental pathology and development. The drivers of said placental abnormalities remain entirely unknown. Given the importance of inflammation and maternal-feto tolerance in proper placental development, thus sought to characterize placental immune profiles in nitrofen- and surgically-induced CDH rat models.
Study Design:
Pregnant Sprague Dawley rats were either treated with nitrofen (via gavage feeding) at embryonic day 9.5 (E9.5) or underwent surgical creation of CDH at E18.5. Placentas were harvested at E21.5. Fetuses were assigned to the groups according to CDH presence in both models. Rat fetuses that were not exposed to nitrofen or surgery were used as controls (CNT). Histological evaluation was performed on the lungs and placentas. Additionally, placentas were used for proteomics analysis.
Results:
Macroscopic inspection of the diaphragm and lung histology confirmed CDH presence and lung hypoplasia. Preliminary proteomics analysis revealed 21 immune system-related proteins as differentially abundant in nitrofen groups and 30 in surgical groups. Four proteins were differentially abundant in both nitrofen and surgical groups relative to controls (Table 1). ARHG2 and CCN2 were elevated in nitrofen groups, and decreased in the surgical groups. CCL4 was decreased in the nitrofen groups, and it was elevated in the surgical groups. In the nitrofen groups, IL1A was increased, while in the surgical groups, it was decreased in abundance.
Conclusion:
This study is the first to identify placental cytokine profiles in nitrofen and surgical CDH rat models. The findings showed distinct immunological responses according to the method of CDH induction, and highlighted key immunological factors linking placental disruptions in CDH, which had not been previously described. Future research is needed to investigate these differences to establish a deeper association between placental disruptions and CDH.