2011

Datson, N.A., Polman, J.A., de Jonge, R.T., van Boheemen, P.T., van Maanen, E.M., Welten, J., McEwen, B.S., Meiland, H.C., Meijer, O.C. , Specific regulatory motifs predict glucocorticoid responsiveness of hippocampal gene expression, Endocrinology, vol. 152, no. 10, pp. 3749-3757.

2010

Sarabdjitsingh, R.A., Isenia, S., Polman, J.A., Mijalkovic, J., Lachize, S.B., Datson, N.A., de Kloet, E.R., Meijer, O.C. , Disrupted corticosterone pulsatile patterns attenuate responsiveness to glucocorticoid signaling in rat brain, Endocrinology, vol. 151, no. 3, pp. 1177-1186.

Van Batenburg, M.F., Li, H., Polman, J.A., Lachize, S.B., Datson, N.A., Bussemaker, H.J., Meijer, O.C. , Paired hormone response elements predict caveolin-1 as a glucocorticoid target gene, PLoS One, vol. 5, no. 1, pp. 1-9.

2009

Richardson, M.K., Gobes, S.M., van Leeuwen, A.C., Polman, J.A., Pieau, C., Sanchez-Villagra, M.R. , Heterochrony in limb evolution: developmental mechanisms and natural selection, J Exp Zool B Mol Dev Evol, vol. 312, no. 6, pp. 639-664.

2008

Bevan, H.S., van den Akker, N.M., Qiu, Y., Polman, J.A., Foster, R.R., Yem, J., Nishikawa, A., Satchell, S.C., Harper, S.J., Gittenberger-de Groot, A.C., Bates, D.O. , The alternatively spliced anti-angiogenic family of VEGF isoforms VEGFxxxb in human kidney development, Nephron Physiol, vol. 110, no. 4, pp. 57-67.

2006

Bekker, M.N., van den Akker, N.M., Bartelings, M.M., Arkesteijn, J.B., Fischer, S.G., Polman, J.A., Haak, M.C., Webb, S., Poelmann, R.E., van Vugt, J.M., Gittenberger-de Groot, A.C. , Nuchal edema and venous-lymphatic phenotype disturbance in human fetuses and mouse embryos with aneuploidy, J Soc Gynecol Investig, vol. 13, no. 3, pp. 209-216.

Identification of epigenetic changes of glucocorticoid-related pathways shaping susceptibility to stress-related psychiatric disorders

It is becoming clear that early life stress may have long-lasting effects on a person’s susceptibility to develop stress-related diseases such as depression. This susceptibility is likely to be caused by stress-induced epigenetic changes that affect gene-expression patterns of stress-responsive genes and eventually the functioning of the stress-system in genetically predisposed individuals. The primary aim of this project is to identify the genes that are susceptible for long-lasting epigenetic changes induced by early life adverse events. To achieve this, we will apply Chromatin immunoprecipitation, followed by sequencing (ChIPseq) that enables large scale analysis of brain binding sites of the GR throughout the genome in an unbiased manner. In this perspective, the genetic pathways that are regulated by the stress-induced Glucocorticoid Receptor (GR) will receive primary focus.