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Clinical and Experimental Obstetrics & Gynecology  2017, Vol. 44 Issue (6): 914-922    DOI: 10.12891/ceog3816.2017
Original Research Previous articles | Next articles
Paternal contribution to the preeclampsia phenotype
T. Tsunemi1, T. Sado1, K. Naruse1, H. Kobayashi1, *()
1 Department of Obstetrics and Gynecology, Nara Medical University, Nara, Japan
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Abstract  
Purpose of investigation: The aims of this study were to elucidate functional pathways of genes responsible for key events in trophoblast invasion and to compare differences in paternal and maternal fitness gene expression in preeclampsia (PE) placenta. Materials and Methods: The authors combined data across seven studies published between 1995 and 2014. All genes downloaded from public web sites were analyzed using the metaprofiling and highlighted differentially expressed genes, the chromosomal location of the candidate genes, enriched pathways, and genomic conflicting situations that may play an important role in the trophoblast invasion. Results: The majority of differentially expressed genes and their downstream targets associated with trophoblast invasion were mediated through the activation of MMP signaling pathways. The paternal fitness genes that favor trophoblast invasion and fetal growth were reduced in the PE placenta. Half of the differentially expressed genes were located in close proximity to known imprinted genes. Several genes identified in PE were located in a cluster of imprinted genes on chromosomes 1p31, 9q34, and 11p15.4. Conclusion: PE may be recognized as a paternal/fetal imprinting disease.
Key words:  Preeclampsia      Trophoblast      Invasion      Imprinting      Matrix metalloproteinase     
Published:  10 December 2017     
*Corresponding Author(s):  H. KOBAYASHI     E-mail:  hirokoba@naramed-u.ac.jp

Cite this article: 

T. Tsunemi, T. Sado, K. Naruse, H. Kobayashi. Paternal contribution to the preeclampsia phenotype. Clinical and Experimental Obstetrics & Gynecology, 2017, 44(6): 914-922.

URL: 

https://ceog.imrpress.com/EN/10.12891/ceog3816.2017     OR     https://ceog.imrpress.com/EN/Y2017/V44/I6/914

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