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dc.contributor.authorLøset, M.
dc.contributor.authorMundal, S.
dc.contributor.authorJohnson, M.
dc.contributor.authorFenstad, M.
dc.contributor.authorFreed, K.
dc.contributor.authorLian, I.
dc.contributor.authorEide, I.
dc.contributor.authorBjørge, L.
dc.contributor.authorBlangero, J.
dc.contributor.authorMoses, Eric
dc.contributor.authorAustgulen, R.
dc.identifier.citationLøset, M. and Mundal, S. and Johnson, M. and Fenstad, M. and Freed, K. and Lian, I. and Eide, I. et al. 2011. A transcriptional profile of the decidua in preeclampsia. American Journal of Obstetrics and Gynecology. 204 (1): pp. 84.e1-84.e27.

OBJECTIVE: We sought to obtain insight into possible mechanisms underlying preeclampsia using genomewide transcriptional profiling in decidua basalis. STUDY DESIGN: Genomewide transcriptional profiling was performed on decidua basalis tissue from preeclamptic (n = 37) and normal (n = 58) pregnancies. Differentially expressed genes were identified and merged into canonical pathways and networks. RESULTS: Of the 26,504 expressed transcripts detected, 455 were differentially expressed (P < .05; false discovery rate, P < .1). Both novel (ARL5B, SLITRK4) and previously reported preeclampsia-associated (PLA2G7, HMOX1) genes were identified. Pathway analysis revealed that tryptophan metabolism, endoplasmic reticulum stress, linoleic acid metabolism, notch signaling, fatty acid metabolism, arachidonic acid metabolism, and NRF2-mediated oxidative stress response were overrepresented canonical pathways. CONCLUSION: In the present study single genes, canonical pathways, and gene-gene networks that are likely to play an important role in the pathogenesis of preeclampsia have been identified. Future functional studies are needed to accomplish a greater understanding of the mechanisms involved.

dc.titleA transcriptional profile of the decidua in preeclampsia
dc.typeJournal Article
dcterms.source.titleAmerican Journal of Obstetrics and Gynecology
curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusFulltext not available

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