NDLI: Activation of Villous Trophoblastic p38 and ERK1/2 Signaling Pathways in Preterm Preeclampsia and HELLP Syndrome

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Activation of Villous Trophoblastic p38 and ERK1/2 Signaling Pathways in Preterm Preeclampsia and HELLP Syndrome

Content Provider	Springer Nature Link
Author	Szabo, Szilvia Mody, Meera Romero, Roberto Xu, Yi Karaszi, Katalin Mihalik, emi Xu, Zhonghui Bhatti, Gaurav Fule, Tibor Hupuczi, Petronella Krenacs, Tibor Rigo, Jas Tarca, Adi L. Hassan, Sonia S. Chaiworapongsa, Tinnakorn Kovalszky, Ilona Papp, Zoltan Than, Nandor Gabor
Copyright Year	2014
Abstract	Preterm preeclampsia is associated with the failure of trophoblast invasion, placental hypoxic/ischemic injury and the release of toxic substances, which promote the terminal pathway of preeclampsia. In term preeclampsia, factors yet unknown trigger the placenta to induce the terminal pathway. The contribution of the villous trophoblast to these pathologic events has not been fully elucidated. Here we aimed to study how stress and signaling pathways influence trophoblastic functions in various subforms of preeclampsia. Tissue microarrays (TMAs) were constructed from placentas obtained from pregnant women in the following groups: 1–2) preterm preeclampsia with (n = 8) or without (n = 7) HELLP syndrome; 3) late-onset preeclampsia (n = 8); 4–5) preterm (n = 5) and term (n = 9) controls. TMA slides were stained for phosphorylated Akt-1, ERK1/2, JNK, and p38 kinases, and trophoblastic immunostainings were semi-quantitatively evaluated. BeWo cells were kept in various stress conditions, and the expression of FLT1, GCM1, LEP, and PGF was profiled by qRT-PCR, while Akt-1, ERK1/2, JNK, and p38 kinase activities were measured with phospho-kinase immunoassays. We found that: 1) Placental LEP and FLT1 expression was up-regulated in preterm preeclampsia with or without HELLP syndrome compared to controls; 2) Mean pp38 immunoscore was higher in preterm preeclampsia, especially in cases with HELLP syndrome, than in controls. 3) Mean pERK1/2 immunoscore was higher in preterm preeclampsia with HELLP syndrome than in controls. 4) In BeWo cells, ischemia up-regulated LEP expression, and it increased JNK and decreased ERK1/2 activity. 5) Hypoxia up-regulated FLT1 and down-regulated PGF expression, and it increased ERK1/2, JNK and p38 activity. 6) IL-1β treatment down-regulated PGF expression, and it increased JNK and p38 activity. 7) The p38 signaling pathway had the most impact on LEP, FLT1 and PGF expression. In conclusion, hypoxic and ischemic stress, along with unknown factors, activates trophoblastic p38 signaling, which has a key role in villous trophoblastic functional changes in preterm preeclampsia. The activation of ERK1/2 signaling may induce additional trophoblastic functional changes in HELLP syndrome, while distinct mechanisms may promote late-onset preeclampsia.
Starting Page	659
Ending Page	668
Page Count	10
File Format	PDF
ISSN	12194956
Journal	Pathology & Oncology Research
Volume Number	21
Issue Number	3
e-ISSN	15322807
Language	English
Publisher	Springer Netherlands
Publisher Date	2015-01-13
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Anti-angiogenic factor Hypertension Mitogen activated protein kinase Oxidative stress Pregnancy Signal transduction Syncytiotrophoblast Cancer Research Oncology Pathology Immunology Biomedicine general
Content Type	Text
Resource Type	Article
Subject	Cancer Research Pathology and Forensic Medicine Oncology

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