Research Article Molecular Patterns of Neurodevelopmental Preconditioning: A Study of the Effects of Antenatal Steroid Therapy in a Protein-Restriction Mouse Model Clarissa Velayo, 1 Takuya Ito, 2 Yupeng Dong, 1 Miyuki Endo, 1 Rika Sugibayashi, 1 Kiyoe Funamoto, 1 Keita Iida, 1 Nobuo Yaegashi, 1 and Yoshitaka Kimura 1,2 1 Department of Obstetrics & Gynecology, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aoba-ku, Sendai, Miyagi 980-8574, Japan 2 International Advanced Research and Education Organization, Tohoku University, Sendai, Miyagi 980-8574, Japan Correspondence should be addressed to Clarissa Velayo; chinkeyvelayo@yahoo.com and Yoshitaka Kimura; ykimura@med.tohoku.ac.jp Received 9 December 2013; Accepted 25 December 2013; Published 13 March 2014 Academic Editors: R. Kimmig, C. J. Petry, and K. Yang Copyright © 2014 Clarissa Velayo et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. Prenatal programming secondary to maternal protein restriction renders an inherent susceptibility to neural compromise in neonates and any addition of glucocorticosteroids results in further damage. Tis is an investigation of consequent global gene activity due to efects of antenatal steroid therapy on a protein restriction mouse model. Methods. C57BL/6N pregnant mice were administered control or protein restricted diets and subjected to either 100 g/Kg of dexamethasone sodium phosphate with normosaline or normosaline alone during late gestation (E10–E17). Nontreatment groups were also included. Brain samples were collected on embryonic day 17 and analyzed by mRNA microarray analysis. Results. Microarray analyses presented 332 signifcantly regulated genes. Overall, neurodevelopmental genes were overrepresented and a subset of 8 genes allowed treatment segregation through the hierarchical clustering method. Te addition of stress or steroids greatly afected gene regulation through glucocorticoid receptor and stress signaling pathways. Furthermore, diferences between dexamethasone-administered treatments implied a harmful efect during conditions of high stress. Microarray analysis was validated using qPCR. Conclusion. Te efects of antenatal steroid therapy vary in fetuses according to maternal-fetal factors and environmental stimuli. Defning the key regulatory networks that signal either benefcial or damaging corticosteroid action would result in valuable adjustments to current treatment protocols. 1. Introduction Te concept of the fetal genome is no longer that of a static framework inherited from paternal and maternal sources but a malleable scafold constantly adapting to stimuli. Tis is most evident in studies involving fetal programming due to the efects of nutritional variation and glucocorticoid exposure [1]. Here, we examined the resulting fetal molec- ular preconditioning due to antenatal steroid therapy using a protein-restriction mouse model. Tis model was frst designed in a previous study [2] as a novel approach to evaluate postnatal adaptive responses due to varied prenatal nutritional conditions and the addition of stress or steroids. Molecular evidence revealed that prenatal programming sec- ondary to maternal protein restriction rendered an inherent susceptibility to neural compromise in neonates and any further addition of antenatal steroids may be detrimental to these already injury-prone ofspring. Tus, an examination of underlying molecular mechanisms in the fetus was warranted to elucidate the efects seen postnatally. Understanding any subtle changes in the fetus induced by these factors and their correlation with phenotypic outcomes in the adult would facilitate early detection of either well- being or disease. Current biomolecular techniques such as microarray analysis have allowed the investigation of global gene expression and subsequently, the parallel data mining Hindawi Publishing Corporation ISRN Obstetrics and Gynecology Volume 2014, Article ID 193816, 13 pages http://dx.doi.org/10.1155/2014/193816