TY - JOUR
T1 - The Effects of Prenatal Iron Deficiency and Risperidone Treatment on the Rat Frontal Cortex
T2 - A Proteomic Analysis
AU - Farrelly, Lorna
AU - Rosato-Siri, Maria Victoria
AU - Föcking, Melanie
AU - Codagnone, Martin
AU - Reines, Analia
AU - Dicker, Patrick
AU - Wynne, Kieran
AU - Farrell, Michael
AU - Cannon, Mary
AU - Cagney, Gerard
AU - Pasquini, Juana Maria
AU - Cotter, David R.
N1 - Funding Information:
Lorna Farrelly, Maria Victoria Rosato-Siri,and Melanie Föcking contributed equally to this work. Juana Maria Pasquini and David R. Cotter are both senior authors of this paper. This study was supported by a grant from Science Foundation Ireland (grant no. RFP1304) and a Health Research Board Clinician Scientist Award to D.R. Cotter and a grant from the University of Buenos Aires (UBA 20020100100395) to J.M. Pasquini. Access to the MS equipment in the Conway Institute and the input of Dr. Jane A. English is gratefully acknowledged.
Publisher Copyright:
© 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
PY - 2017/9
Y1 - 2017/9
N2 - Prenatal iron deficiency (pID) has been described to increase the risk for neurodevelopmental disorders such as autism and schizophrenia; however, the precise molecular mechanisms are still unknown. Here, we utilized high-throughput MS to examine the proteomic effects of pID in adulthood on the rat frontal cortex area (FCA). In addition, the FCA proteome was examined in adulthood following risperidone treatment in adolescence to see if these effects could be prevented. We identified 1501 proteins of which 100 were significantly differentially expressed in the FCA at postnatal day 90. Pathway analysis of proteins affected by pID revealed changes in metabolic processes, including the tricyclic acid cycle, mitochondrial dysfunction, and P13K/Akt signaling. Interestingly, most of these protein changes were not present in the adult pID offspring who received risperidone in adolescence. Considering the link between pID and several neurodevelopmental disorders such as autism and schizophrenia these presented results bring new perspectives to understand the role of iron in metabolic pathways and provide novel biomarkers for future studies of pID.
AB - Prenatal iron deficiency (pID) has been described to increase the risk for neurodevelopmental disorders such as autism and schizophrenia; however, the precise molecular mechanisms are still unknown. Here, we utilized high-throughput MS to examine the proteomic effects of pID in adulthood on the rat frontal cortex area (FCA). In addition, the FCA proteome was examined in adulthood following risperidone treatment in adolescence to see if these effects could be prevented. We identified 1501 proteins of which 100 were significantly differentially expressed in the FCA at postnatal day 90. Pathway analysis of proteins affected by pID revealed changes in metabolic processes, including the tricyclic acid cycle, mitochondrial dysfunction, and P13K/Akt signaling. Interestingly, most of these protein changes were not present in the adult pID offspring who received risperidone in adolescence. Considering the link between pID and several neurodevelopmental disorders such as autism and schizophrenia these presented results bring new perspectives to understand the role of iron in metabolic pathways and provide novel biomarkers for future studies of pID.
KW - Antipsychotics
KW - Environmental risk factor
KW - Myelination
KW - Schizophrenia
UR - http://www.scopus.com/inward/record.url?scp=85029889115&partnerID=8YFLogxK
U2 - 10.1002/pmic.201600407
DO - 10.1002/pmic.201600407
M3 - Article
C2 - 28762254
AN - SCOPUS:85029889115
SN - 1615-9853
VL - 17
JO - Proteomics
JF - Proteomics
IS - 17-18
M1 - 1600407
ER -