Differential activation of placental unfolded protein response pathways implies heterogeneity in causation of early- and late-onset pre-eclampsia

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Yung, Hong Wa (author)

Differential activation of placental unfolded protein response pathways implies heterogeneity in causation of early- and late-onset pre-eclampsia

Article/chapterEnglish2014

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2014-08-06
Wiley,2014
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LIBRIS-ID:oai:DiVA.org:uu-236057
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-236057URI
https://doi.org/10.1002/path.4394DOI

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Language:English
Summary in:English

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Based on gestational age at diagnosis and/or delivery, pre-eclampsia (PE) is commonly divided into early-onset (<34 weeks) and late-onset (>= 34 weeks) forms. Recently, the distinction between 'placental' and 'maternal' causation has been proposed, with 'placental' cases being more frequently associated with early-onset and intrauterine growth restriction. To test whether molecular placental pathology varies according to clinical presentation, we investigated stress-signalling pathways, including unfolded protein response (UPR) pathways, MAPK stress pathways, heat-shock proteins and AMPK.. in placentae delivered by caesarean section for clinical indications at different gestational ages. Controls included second-trimester, pre-term and normal-term placentae. BeWo cells were used to investigate how these pathways react to different severities of hypoxia-reoxygenation (H/R) and pro-inflammatory cytokines. Activation of placental UPR and stress-response pathways, including P-IRE1 alpha, ATF6, XBP-1, GRP78 and GRP94, P-p38/p38 and HSP70, was higher in early-onset PE than in both late-onset PE and normotensive controls (NTCs), with a clear inflection around 34 weeks. Placentae from >= 34 weeks PE and NTC were indistinguishable. Levels of UPR signalling were similar between second-trimester and term controls, but were significantly higher in pre-term 'controls' delivered vaginally for chorioamnionitis and other conditions. Severe H/R (1/20% O-2) induced equivalent activation of UPR pathways, including P-eIF2 alpha, ATF6, P-IRE1 alpha, GRP78 and GRP94, in BeWo cells. By contrast, the pro-inflammatory cytokines TNF alpha and IL-1 beta induced only mild activation of P-eIF2 alpha and GRP78. AKT, a central regulator of cell proliferation, was reduced in the <34 weeks PE placentae and severe H/R-treated cells, but not in other conditions. These findings provide the first molecular evidence that placental stress may contribute to the pathophysiology of early-onset pre-eclampsia, whereas that is unlikely to be the case in the late-onset form of the syndrome. (c) 2014 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Cancer och onkologi hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology hsv//eng
placenta
pre-eclampsia
pregnancy
growth restriction
cell stress responses
unfolded protein response

Added entries (persons, corporate bodies, meetings, titles ...)

Atkinson, Daniel (author)
Campion-Smith, TimUppsala universitet,Institutionen för kvinnors och barns hälsa (author)
Olovsson, MattsUppsala universitet,Obstetrik & gynekologi(Swepub:uu)mattolov (author)
Charnock-Jones, D. Stephen (author)
Burton, Graham J. (author)
Uppsala universitetInstitutionen för kvinnors och barns hälsa (creator_code:org_t)

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In:Journal of Pathology: Wiley234:2, s. 262-2760022-34171096-9896

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