ArticleHypertension (Dallas, Tex. : 1979)2019
Proteasome Levels and Activity in Pregnancies Complicated by Severe Preeclampsia and Hemolysis, Elevated Liver Enzymes, and Thrombocytopenia (HELLP) Syndrome.
Article in Hypertension (Dallas, Tex. : 1979), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Placental changes with assisted reproductive technologies: insights from the transcriptomic and proteomic profiling of multiple species.Journal of animal science · 2026Review
- Causal relationship between hepatic function indicators and thrombocytopenia risk in early-stage hepatitis B virus infection: evidence from clinical observational studies and mendelian randomization analyses.Frontiers in immunology · 2025Observational
- Antineoplastic Properties by Proapoptotic Mechanisms Induction ofBiomedicines · 2022Review
- Bioinformatics analysis of microarray data to identify hub genes, as diagnostic biomarker of HELLP syndrome: System biology approach.The journal of obstetrics and gynaecology research · 2022Article
- Conformation-dependent anti-Aβ monoclonal antibody signatures of disease status and severity in urine of women with preeclampsia.Pregnancy hypertension · 2022Article
- The ATP/MgMethods and protocols · 2022Article
- Integrated genomic analysis of proteasome alterations across 11,057 patients with 33 cancer types: clinically relevant outcomes in framework of 3P medicine.The EPMA journal · 2021Article
- Article
- Amniotic Fluid Proteasome and Immunoproteasome in the Setting of Intra-Amniotic Infection, Inflammation, and Preterm Birth.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Dissecting human trophoblast cell transcriptional heterogeneity in preeclampsia using single-cell RNA sequencing.Molecular genetics & genomic medicine · 2021Article
- Protein Network Analysis of Whole Exome Sequencing of Severe Preeclampsia.Frontiers in genetics · 2021Article
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6 authors at 1 institution in 1 country.
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Abstract
Excessive accumulation of misfolded proteins was recently demonstrated in preeclampsia. We examined levels and activity of circulatory proteasome and immunoproteasome (inflammatory subtype) in preeclampsia and hemolysis, elevated liver enzymes, and thrombocytopenia (HELLP) syndrome. We analyzed samples from women with hypertensive pregnancy disorders (n=115), including preeclampsia with severe features (sPE) and HELLP syndrome, and normotensive controls (n=45). Plasma proteasome and immunoproteasome immunoreactivity were determined by quantifying the α-subunit of the 20S core and β5i (proteasome subunit beta 8 [PSMB8]), respectively. Plasma proteasome activity was analyzed with fluorogenic substrates. MG132, lactacystin, and ONX0914 were used to inhibit the circulating proteasome and immunoproteasome, respectively. Plasma cytokine profiles were evaluated by multiplex immunoassay. Placental expression of β5 (constitutive proteasome) and β5i (immunoproteasome) was interrogated by immunohistochemistry. Women with sPE had increased plasma 20S levels ( P<0.001) and elevated lytic activities (chymotrypsin-like 7-fold, caspase-like 4.2-fold, trypsin-like 2.2-fold; P <0.001 for all) compared with pregnant controls. Women with features of HELLP displayed the highest plasma proteasome levels and activity, which correlated with decreased IFN-γ (interferon-γ), and increased IL (interleukin)-8 and IL-10. In sPE and HELLP, chymotrypsin-like activity was suppressed by proteasome inhibitors including ONX0914. Compared with gestational age-matched controls, sPE placentas harbored increased β5 and β5i immunostaining in trophoblasts. β5i signal was elevated in HELLP with predominant staining in villous core, extravillous trophoblasts in placental islands, and extracellular vesicles in intervillous spaces. Pregnancy represents a state of increased proteostatic stress. sPE and HELLP were characterized by significant upregulation in circulating levels and lytic activity of the proteasome that was partially explained by placental immunoproteasome upregulation.
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