Implications of maternal systemic oxidative stress in normal pregnancy and in pregnancy complicated by preeclampsia

Mihu, Dan; Sabau, L.; Costin, Nicolae; Ciortea, Răzvan; Măluţan, Andrei Mihai; Mihu, Carmen Mihaela

doi:10.3109/14767058.2011.600796

Cited by 24 publications

(14 citation statements)

References 48 publications

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“…Two hypotheses can be invoked to explain these findings. First, a higher plasma sST2 concentration may be a consequence of an intravascular inflammatory response which is exacerbated in preeclampsia when compared to an uncomplicated pregnancy [23,25,[168][169][170]. Indeed, it has been demonstrated that pro-inflammatory cytokines are increased in the plasma or serum of women with early-onset preeclampsia [35,41,42] and severe preeclampsia [36,40,41] when compared to women with uncomplicated pregnancies.…”

Section: Plasma Concentrations Of Soluble St2 Is Elevated In Preeclammentioning

confidence: 99%

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Stampalija

Chaiworapongsa

Romero

et al. 2013

The Journal of Maternal-Fetal & Neonatal Medicine

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Objectives: Angiogenic/anti-angiogenic factors have emerged as one of the promising biomarkers for the prediction of preeclampsia. Since not all patients with preeclampsia can be identified by these analytes, the search for additional biomarkers continues. The soluble form of ST2 (sST2), a protein capable of binding to interleukin (IL)-33 and thus contributing to a Th1-biased immune response, has been reported to be elevated in maternal plasma of women with preeclampsia. The aims of this study were to examine: (1) differences in maternal plasma concentrations of sST2 and IL-33 between women diagnosed with preeclampsia and those having uncomplicated pregnancies; (2) the relationship between sST2, umbilical and uterine artery Doppler velocimetry, and the severity of preeclampsia; and (3) the performance of sST2 and angiogenic/anti-angiogenic factors in identifying patients with preeclampsia at the time of diagnosis. Methods: This cross-sectional study included women with preeclampsia (n ¼ 106) and women with an uncomplicated pregnancy (n ¼ 131). Plasma concentrations of sST2, IL-33, soluble vascular endothelial growth factor receptor (sVEGFR)-1, soluble endoglin (sEng) and placental growth factor (PlGF) were determined by enzyme linked immune sorbent assay. Area under the receiver operating characteristic curve (AUC) for the identification of preeclampsia was examined for each analyte. Results: (1) Patients with preeclampsia had a higher mean plasma concentrations of sST2 than those with an uncomplicated pregnancy (p50.0001), while no significant difference in the mean plasma concentration of IL-33 between the two groups was observed; (2) the magnitude of this difference was greater in early-onset, compared to late-onset disease, and in severe compared to mild preeclampsia; (3) sST2 plasma concentrations did not correlate with the results of uterine or umbilical artery Doppler velocimetry (p ¼ 0.7 and p ¼ 1, respectively) among women with preeclampsia; (4) sST2 correlated positively with plasma concentrations of sVEGFR1-1 and sEng (Spearman's Rho ¼ 0.72 and 0.63; each p50.0001), and negatively with PlGF (Spearman's Rho ¼ À0.56, p50.0001); and (5) while the AUC achieved by sST2 and angiogenic/anti-angiogenic factors in identifying women with preeclampsia at the time of diagnosis were non-significantly different prior to term (537 weeks of gestation), thereafter the AUC achieved by sST2 was significantly less than that achieved by angiogenic/anti-angiogenic factors. Conclusions: Preeclampsia is associated with increased maternal plasma concentrations of sST2. The findings that sST2 concentrations do not correlate with uterine or umbilical artery Doppler velocimetry in women with preeclampsia suggest that elevated maternal plasma sST2 concentrations in preeclampsia are not related to the increased impedance to flow in the uteroplacental circulation. The performance of sST2 in identifying preeclampsia at the time of diagnosis prior to 37 weeks of gestation was comparable to that of angiogenic/anti-angiogenic f...

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Section: Plasma Concentrations Of Soluble St2 Is Elevated In Preeclammentioning

confidence: 99%

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Stampalija

Chaiworapongsa

Romero

et al. 2013

The Journal of Maternal-Fetal & Neonatal Medicine

View full text Add to dashboard Cite

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“…A study performed by McCormick et al supported the finding that an increase in the permeability of capillaries may cause vasogenic edema and cortical blindness as a result (17). Complement activation and leucocyte aggregation lead to the formation of emboli in the retinal arterioles and manifest as Purtscher retinopathy (18).…”

Section: Pathophysiologymentioning

confidence: 94%

Preeclampsia Induced Ocular Change

Ghavidel¹,

Mousavi²,

Bagheri³

et al. 2017

International Journal of Women’s Health and Reproduction Scienc

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“…These immune cells, released upon placental ischemia can generate superoxide within the maternal vascular endothelium 7 . Indeed increased levels of ROS and 8-isoPGF2α, the free form of isoprostane, are found in placentas and in the circulation of women with preeclampsia 8, 9 , indicating that preeclampsia is accompanied by an increase in pro-oxidant factors. During hypertensive disorders peroxynitrite concentrations 10, 11 and ROS are also released by the maternal vascular endothelium and smooth muscle cells (SMC) stimulated by stress or angiotensin II.…”

Section: Introductionmentioning

confidence: 99%

CD4 ⁺ T Cells Are Important Mediators of Oxidative Stress That Cause Hypertension in Response to Placental Ischemia

et al. 2014

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Preeclampsia is associated with oxidative stress which is suspected to play a role in hypertension, placental ischemia and fetal demise associated with the disease. Various cellular sources of oxidative stress such as neutrophils, monocytes and CD4+T cells have been suggested as culprits in the pathophysiology of preeclampsia. The objective of this study was to examine a role for circulating and placental CD4+T cells in oxidative stress in response to placental ischemia during pregnancy. CD4+T cells and oxidative stress was measured in preeclamptic and normal pregnant women, placental ischemic and normal pregnant rats and normal pregnant recipient rats of placental ischemic CD4+ T cells. Preeclamptic women had significantly increased circulating (p=0.02) and placental CD4+T cells (p=0.0001); lymphocyte secretion of myeloperoxidase (p=0.004); and placental reactive oxygen species (p=0.0004) compared to normal pregnant women. CD4+T cells from placental ischemic rats cause many facets of preeclampsia when injected into normal pregnant recipient rats on gestational day 13. On gestational day 19 blood pressure increased in normal pregnant recipients of placental ischemic CD4+T cells (p=0.002) compared to normal pregnant rats. Similar to preeclamptic patients, CD4+ T cells from placental ischemic rats secreted significantly more myeloperoxidase (p=0.003) and induced oxidative stress in cultured vascular cells (p=0.003) than normal pregnant rat CD4+Tcells. Apocynin, an NADPH inhibitor, attenuated hypertension, and all oxidative stress markers in placental ischemic and normal pregnant recipient rats of placental ischemic CD4+Tcells (p=0.05). These data demonstrate an important role for CD4+T cells in mediating another factor, oxidative stress, to cause hypertension during preeclampsia.

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Implications of maternal systemic oxidative stress in normal pregnancy and in pregnancy complicated by preeclampsia

Abstract: Oxidative stress in preeclampsia is the result of the increase in reactive oxygen species and of the decrease in antioxidants.

Cited by 24 publications

References 48 publications

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Preeclampsia Induced Ocular Change

CD4 ⁺ T Cells Are Important Mediators of Oxidative Stress That Cause Hypertension in Response to Placental Ischemia

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Implications of maternal systemic oxidative stress in normal pregnancy and in pregnancy complicated by preeclampsia

Abstract: Oxidative stress in preeclampsia is the result of the increase in reactive oxygen species and of the decrease in antioxidants.

Cited by 24 publications

References 48 publications

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Preeclampsia Induced Ocular Change

CD4 + T Cells Are Important Mediators of Oxidative Stress That Cause Hypertension in Response to Placental Ischemia

Contact Info

Product

Resources

About

CD4 ⁺ T Cells Are Important Mediators of Oxidative Stress That Cause Hypertension in Response to Placental Ischemia