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Preeclampsia: increased expression of soluble ADAM 12

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Abstract

Preeclampsia is a multisystemic pregnancy-associated disease affecting about 3–7% of pregnancies worldwide and is still a principal cause of fetal and maternal morbidity and mortality. To identify potential markers, we have compared gene expression profiles from control and preeclamptic placental tissues taken at various age-matched gestational stages using complementary DNA microarray analysis. Besides previously identified preeclampsia-associated genes, novel differentially expressed transcripts were found. The soluble form of the disintegrin metalloprotease ADAM 12 (a disintegrin and metalloproteinase 12; meltrin-α) represented the most upregulated transcript. This was confirmed by in situ hybridization of sections of preeclamptic placentas and by serum protein analysis of preeclamptic pregnant women. Thus, ADAM 12 could serve as an early biomarker for preeclampsia that may be of predictive and/or functional significance.

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Abbreviations

ADAM 12:

a disintegrin and metalloproteinase 12

EBI3 :

Epstein–Barr virus-induced gene 3

IGF:

insulin-like growth factor

IGFBP:

insulin-like-growth-factor-binding protein

LIM/LHX:

LIM homeobox domain protein

MIFR-2:

metalloproteinase in the female reproductive tract 2

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Acknowledgements

We are grateful to Prof. U.M. Wewer for kind provision of the rb122 antibody, Dr. S. Stumm for filing of patient data, and the midwives on duty for their support. We thank S. Adams and T. Raubinger for excellent technical assistance and Drs. J. Hess, A. Kolbus, and H. Richter for helpful discussions and critical reading of the manuscript. This work was supported by the Training and Mobility of Researchers Programs of the European Economic Community and by the Deutsche Forschungsgemeinschaft (Scho 365/2-4).

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Correspondence to Marina Schorpp-Kistner.

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Sabine Gack, Alexander Marmé, and Frederik Marmé contributed equally to this work

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Gack, S., Marmé, A., Marmé, F. et al. Preeclampsia: increased expression of soluble ADAM 12. J Mol Med 83, 887–896 (2005). https://doi.org/10.1007/s00109-005-0714-9

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