Microarray profiling reveals that placental transcriptomes of early-onset HELLP syndrome and preeclampsia are similar

T. Várkonyi, B. Nagy, T. Füle, A. L. Tarca, K. Karászi, J. Schönléber, P. Hupuczi, N. Mihalik, I. Kovalszky, J. Rigó, H. Meiri, Z. Papp, R. Romero, N. G. Than

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Abstract

Background: The involvement of the placenta in the pathogenesis of preeclampsia and HELLP syndrome is well established, and placental lesions are also similar in these two syndromes. Here we aimed to examine the placental transcriptome and to identify candidate biomarkers in early-onset preeclampsia and HELLP syndrome. Methods: Placental specimens were obtained at C-sections from women with early-onset preeclampsia and HELLP syndrome, and from controls who delivered preterm or at term. After histopathological examination, fresh-frozen placental specimens were used for microarray profiling and validation by qRT-PCR. Differential expression was analysed using log-linear models while adjusting for gestational age. Gene ontology and pathway analyses were used to interpret gene expression changes. Tissue microarrays were constructed from paraffin-embedded placental specimens and immunostained. Results: Placental gene expression was gestational age-dependent among preterm and term controls. Out of the 350 differentially expressed genes in preeclampsia and 554 genes in HELLP syndrome, 224 genes (including LEP, CGB, LHB, INHA, SIGLEC6, PAPPA2, TREM1, and FLT1) changed in the same direction (elevated or reduced) in both syndromes. Many of these encode proteins that have been implicated as biomarkers for preeclampsia. Enrichment analyses revealed similar biological processes, cellular compartments and biological pathways enriched in early-onset preeclampsia and HELLP syndrome; however, some processes and pathways (e.g., cytokine-cytokine receptor interaction) were over-represented only in HELLP syndrome. Conclusion: High-throughput transcriptional and tissue microarray expression profiling revealed that placental transcriptomes of early-onset preeclampsia and HELLP syndrome largely overlap, underlying a potential common cause and pathophysiologic processes in these syndromes. However, gene expression changes may also suggest a more severe placental pathology and pronounced inflammatory response in HELLP syndrome than in preeclampsia.

Original languageEnglish
JournalPlacenta
Volume32
Issue numberSUPPL. 1
DOIs
Publication statusPublished - Feb 2011

Fingerprint

HELLP Syndrome
Pre-Eclampsia
Transcriptome
Gene Expression
Gestational Age
Biomarkers
Genes
Biological Phenomena
Gene Ontology
Cytokine Receptors
Paraffin
Placenta
Linear Models
Pathology
Cytokines
Polymerase Chain Reaction

Keywords

  • Differential expression
  • High-dimensional biology
  • Syncytiotrophoblast
  • Systemic inflammation
  • Virtual microscopy

ASJC Scopus subject areas

  • Obstetrics and Gynaecology
  • Reproductive Medicine
  • Developmental Biology

Cite this

Microarray profiling reveals that placental transcriptomes of early-onset HELLP syndrome and preeclampsia are similar. / Várkonyi, T.; Nagy, B.; Füle, T.; Tarca, A. L.; Karászi, K.; Schönléber, J.; Hupuczi, P.; Mihalik, N.; Kovalszky, I.; Rigó, J.; Meiri, H.; Papp, Z.; Romero, R.; Than, N. G.

In: Placenta, Vol. 32, No. SUPPL. 1, 02.2011.

Research output: Contribution to journalArticle

Várkonyi, T. ; Nagy, B. ; Füle, T. ; Tarca, A. L. ; Karászi, K. ; Schönléber, J. ; Hupuczi, P. ; Mihalik, N. ; Kovalszky, I. ; Rigó, J. ; Meiri, H. ; Papp, Z. ; Romero, R. ; Than, N. G. / Microarray profiling reveals that placental transcriptomes of early-onset HELLP syndrome and preeclampsia are similar. In: Placenta. 2011 ; Vol. 32, No. SUPPL. 1.
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AU - Nagy, B.

AU - Füle, T.

AU - Tarca, A. L.

AU - Karászi, K.

AU - Schönléber, J.

AU - Hupuczi, P.

AU - Mihalik, N.

AU - Kovalszky, I.

AU - Rigó, J.

AU - Meiri, H.

AU - Papp, Z.

AU - Romero, R.

AU - Than, N. G.

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N2 - Background: The involvement of the placenta in the pathogenesis of preeclampsia and HELLP syndrome is well established, and placental lesions are also similar in these two syndromes. Here we aimed to examine the placental transcriptome and to identify candidate biomarkers in early-onset preeclampsia and HELLP syndrome. Methods: Placental specimens were obtained at C-sections from women with early-onset preeclampsia and HELLP syndrome, and from controls who delivered preterm or at term. After histopathological examination, fresh-frozen placental specimens were used for microarray profiling and validation by qRT-PCR. Differential expression was analysed using log-linear models while adjusting for gestational age. Gene ontology and pathway analyses were used to interpret gene expression changes. Tissue microarrays were constructed from paraffin-embedded placental specimens and immunostained. Results: Placental gene expression was gestational age-dependent among preterm and term controls. Out of the 350 differentially expressed genes in preeclampsia and 554 genes in HELLP syndrome, 224 genes (including LEP, CGB, LHB, INHA, SIGLEC6, PAPPA2, TREM1, and FLT1) changed in the same direction (elevated or reduced) in both syndromes. Many of these encode proteins that have been implicated as biomarkers for preeclampsia. Enrichment analyses revealed similar biological processes, cellular compartments and biological pathways enriched in early-onset preeclampsia and HELLP syndrome; however, some processes and pathways (e.g., cytokine-cytokine receptor interaction) were over-represented only in HELLP syndrome. Conclusion: High-throughput transcriptional and tissue microarray expression profiling revealed that placental transcriptomes of early-onset preeclampsia and HELLP syndrome largely overlap, underlying a potential common cause and pathophysiologic processes in these syndromes. However, gene expression changes may also suggest a more severe placental pathology and pronounced inflammatory response in HELLP syndrome than in preeclampsia.

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KW - Virtual microscopy

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