Imbalance of expression of bFGF and PK1 is associated with defective maturation and antenatal placental insufficiency

L. Seidmann, T. Suhan, R. Unger, V. Gerein, C. J. Kirkpatrick

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

Objective: Defective placental maturation is associated with restricted functional capacity and adverse perinatal fetal outcomes. The aim of the study was a comparative analysis of the role of mRNA expression of various angiogenic factors in placental maturation defects. Study design: We examined the mRNA expression patterns of prokineticin 1 (PK1), its receptors (PKRs), basic-fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) in tissue from third-trimester placentae that exhibited delayed or accelerated villous maturation. Results The expression of PK1 and PKR2 was elevated in placental tissue exhibiting accelerated maturation and a predominant differentiation of terminal villi. The opposite was found in tissue exhibiting delayed maturation and deficiency of the terminal villi. In addition, low expression of bFGF correlated with the predominant differentiation of terminal villi, whereas the opposite was observed when terminal villi were deficient. The expression of VEGF, PIGF, and PKR1 showed no significant differences between the groups. Conclusion Defective placental maturation is associated with an imbalance of expression of bFGF and PK1. Our results: demonstrate an involvement of the PK1/PKR2-signalling pathway in the regulation of the functional adequate capillarization in late pregnancy. We propose the bFGF/PK1-ratio as a monitor of placental function and a possible indicator of latent clinical problems, such as placental dysfunction leading to fetal hypoxia.

Original languageEnglish
Pages (from-to)352-357
Number of pages6
JournalEuropean Journal of Obstetrics, Gynecology and Reproductive Biology
Volume170
Issue number2
DOIs
StatePublished - Oct 2013
Externally publishedYes

Bibliographical note

Funding Information:
The authors thank Erik Springer for constructive discussion of molecular biological methods and Nadeshda Homm for excellent technical assistance. This work was kindly supported by the foundation “Dr. Valentin Gerein Stiftung – Hilfe für krebskranke Kinder, Jugendliche, junge Erwachsene”.

Funding

The authors thank Erik Springer for constructive discussion of molecular biological methods and Nadeshda Homm for excellent technical assistance. This work was kindly supported by the foundation “Dr. Valentin Gerein Stiftung – Hilfe für krebskranke Kinder, Jugendliche, junge Erwachsene”.

FundersFunder number
Dr. Valentin Gerein Stiftung

    Keywords

    • Capillarization
    • Fetal hypoxia
    • Maturation defect
    • Placental dysfunction
    • Prokineticin bFGF

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