A clinicohistopathologic comparison between HELLP syndrome and severe preeclampsia

Smulian, John C.; Shen‐Schwarz, Susan; Scorza, William E.; Kinzler, Wendy L.; Vintzileos, Anthony M.

doi:10.1080/14767050400018015

Cited by 12 publications

(7 citation statements)

References 18 publications

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“…These findings are also consistent with reports showing similar changes in placental pathology and global transcriptome in preterm preeclampsia and HELLP syndrome. 16,42,80 These data suggest that the apical, nonlipid raft localization of PP13 in the syncytiotrophoblast brush border is reduced, and the association of PP13 with the juxtamembrane cortical actin network and lipid raft domains is enhanced in preterm preeclampsia and HELLP syndrome by yet unknown mechanism, possibly facilitating the secretion and/or shedding of PP13 through lipid rafts and leading to the elevated PP13 concentrations in the maternal circulation.…”

Section: Commentmentioning

confidence: 85%

Placental protein 13 (PP13/galectin-13) undergoes lipid raft-associated subcellular redistribution in the syncytiotrophoblast in preterm preeclampsia and HELLP syndrome

Balogh¹,

Pozsgay²,

Matkó³

et al. 2011

American Journal of Obstetrics and Gynecology

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Objective To investigate placental protein 13 (PP13) localization in relation to cytoskeleton and lipid rafts in preeclampsia and HELLP syndrome. Study Design Placental cryosections from patients with preeclampsia and HELLP, and controls were stained for PP13, actin, PLAP (lipid raft marker), and CD71 (nonraft marker). BeWo cells exposed to stress conditions were stained for PP13 and actin. Protein localization were investigated by confocal microscopy, PP13 concentrations by ELISA. Results PP13-actin colocalization was increased in syncytiotrophoblast juxtamembrane regions in term/preterm preeclampsia and HELLP. PP13-CD71 colocalization was decreased and PP13-PLAP proximity was increased in preterm but not term preeclampsia and HELLP. PP13-release from BeWo cells was inhibited by cytoskeleton disruption, and augmented by Ca2+-influx and ischemic stress. Conclusion The actin cytoskeleton, probably in connection with lipid rafts, controls trophoblastic “nonclassical” PP13 export. PP13 is released from the syncytiotrophoblast in preterm preeclampsia and HELLP, mimicked in BeWo cells by ischemic stress, suggesting PP13 is a placental alarmin.

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Section: Commentmentioning

confidence: 85%

Placental protein 13 (PP13/galectin-13) undergoes lipid raft-associated subcellular redistribution in the syncytiotrophoblast in preterm preeclampsia and HELLP syndrome

Balogh¹,

Pozsgay²,

Matkó³

et al. 2011

American Journal of Obstetrics and Gynecology

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“…In spite of histological findings in term preeclampsia, more pronounced placental morphological changes are found in early-onset preeclampsia [13,14], in accord with differences in placental gene expression between these two subtypes of preeclampsia [20]. Of interest, placental morphological changes in HELLP syndrome are consistent with those in preeclampsia in early-onset cases [21]. Indeed, previously we also observed a similar degree of histopathological abnormalities in early-onset preeclampsia and HELLP syndrome [22].…”

Section: Disucssionmentioning

confidence: 99%

“…Differences between early- and late-onset preeclampsia have been identified in placental gene expression signatures [20]. When comparing preeclampsia with HELLP syndrome, the frequency of placental histopathological lesions was found to be similar in these two syndromes in a patient group with early-onset diseases [21]. It is possible that a common cause and pathophysiologic processes will lead to shared placental and clinical features in early-onset preeclampsia and HELLP syndrome.…”

Section: Introductionmentioning

confidence: 99%

Microarray Profiling Reveals That Placental Transcriptomes of Early-onset HELLP Syndrome and Preeclampsia Are Similar

et al. 2011

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Background The involvement of the placenta in the pathogenesis of preeclampsia and HELLP syndrome is well established, and placental lesions 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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“…HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome, which is considered to belong to the disease spectrum of preeclampsia (PE) occurs in 0.5–0.9% of all pregnancies and in 10–20% of those with severe PE . It is generally accepted that PE, particularly early onset disease, results from impaired placentation in early gestation, and HELLP syndrome has been shown to share histopathologic, placental morphologic and changes in gene expression with early onset PE . First‐trimester biochemical and biophysical maternal changes observed in pregnancies that develop PE have been used to develop algorithms to estimate the individualized risk of a woman to develop PE.…”

Section: Introductionmentioning

confidence: 99%

First trimester prediction of HELLP syndrome

et al. 2015

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A clinicohistopathologic comparison between HELLP syndrome and severe preeclampsia

Abstract: The significant overlap between HELLP syndrome and severe preeclampsia for both clinical and placental features suggests that the two conditions represent a spectrum of essentially the same pathophysiologic process.

Cited by 12 publications

References 18 publications

Placental protein 13 (PP13/galectin-13) undergoes lipid raft-associated subcellular redistribution in the syncytiotrophoblast in preterm preeclampsia and HELLP syndrome

Placental protein 13 (PP13/galectin-13) undergoes lipid raft-associated subcellular redistribution in the syncytiotrophoblast in preterm preeclampsia and HELLP syndrome

Microarray Profiling Reveals That Placental Transcriptomes of Early-onset HELLP Syndrome and Preeclampsia Are Similar

First trimester prediction of HELLP syndrome

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