Neutrophils from pregnant women produce thromboxane and tumor necrosis factor-α in response to linoleic acid and oxidative stress

Vaughan, John E.; Walsh, Scott W.

doi:10.1016/j.ajog.2005.01.057

Cited by 31 publications

(31 citation statements)

References 21 publications

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“…26,48 Evidence presented in this study suggests that the potential mechanism for MMP-1 induction and activation may involve the generation of ROS and TNF-␣ by infiltrated neutrophils. This notion is supported by studies 13,15,16,49 showing that TNF-␣ and ROS modulate the expression of different MMPs in VSMCs and promote the activation of MMPs secreted by VSMCs.…”

Section: Discussionmentioning

confidence: 81%

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Estrada-Gutiérrez

Cappello

Mishra

et al. 2011

The American Journal of Pathology

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This study was conducted to determine the following: (1) whether matrix metalloproteinase-1 (MMP-1) is increased in systemic vessels of preeclamptic women, (2) whether this increase might be mediated by neutrophils, and (3) whether MMP-1 could be responsible for vascular dysfunction. Omental arteries and plasma were collected from healthy pregnant and preeclamptic women. Omental arteries were evaluated for gene and protein expression of MMP-1, collagen type 1␣, tissue inhibitor of metalloproteinase-1, and vascular reactivity to MMP-1. Gene and protein expression levels were also evaluated in human vascular smooth muscle cells (VSMCs) co-cultured with activated neutrophils, reactive oxygen species, or tumor necrosis factor ␣. Vessel expression of MMP-1 and circulating MMP-1 levels were increased in preeclamptic women, whereas vascular expression of collagen or tissue inhibitor of metalloproteinase-1 were down-regulated or unchanged. In cultured VSMCs, the imbalance in collagen-regulating genes of preeclamptic vessels was reproduced by treatment with neutrophils, tumor necrosis factor ␣, or reactive oxygen species. Chemotaxis studies with cultured cells revealed that MMP-1 promoted recruitment of neutrophils via vascular smooth muscle release of interleukin-8. Furthermore, MMP-1 induced vasoconstriction via protease-activated receptor-1, whose expression was significantly increased in omental arteries of preeclamptic women and in VSMCs co-cultured with neutrophils. Collectively, these findings disclose a novel role for MMP-1 as a mediator of vasoconstriction and vascular dysfunction in preeclampsia.

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Section: Discussionmentioning

confidence: 81%

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Estrada-Gutiérrez

Cappello

Mishra

et al. 2011

The American Journal of Pathology

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“…Oxidized lipids are potent activators of neutrophils and cause their expression of COX-2 which regulates their release of thromboxane, TNFα and superoxide (25,26). Neutrophils obtained from preeclamptic women express significantly more COX-2 than neutrophils obtained from normal pregnant women or normal nonpregnant women (27).…”

Section: Discussionmentioning

confidence: 99%

Neutrophils, but Not Lymphocytes or Monocytes, Infiltrate Maternal Systemic Vasculature in Women with Preeclampsia

Cadden

Walsh

2008

Hypertension in Pregnancy

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Objective-Leukocytes are activated in women with preeclampsia, but the class of leukocytes that infiltrates the maternal vasculature and, therefore, most likely to cause vascular dysfunction is not known.Methods-Subcutaneous fat biopsies were obtained at cesarean section or abdominal surgery from 7 normal nonpregnant women, 7 normal pregnant women, and 7 preeclamptic women. Tissues were immunohistochemically stained for CD14, a monocyte/macrophage antigen, CD99, a lymphocyte antigen, and CD66b, a neutrophil antigen.Results-CD14 stained cells were found infiltrated into fat tissue but were not present in vessels for any of the groups. CD99 stained cells were present in approximately 20-30% of vessels with no difference among groups. CD66b stained cells were present in all groups with a significantly greater percentage of vessels stained for preeclamptic than normal pregnant or normal nonpregnant women (70±6 vs. 43±9 vs. 21±5%, respectively, P<0.01). CD66b cells were the most abundant cell type that infiltrated vessels of preeclamptic women. Conclusions-1)There was significantly more neutrophils adhered to endothelium and infiltrated into the intimal space in the maternal systemic vasculature of preeclamptic women than in normal pregnant women or normal nonpregnant women; 2) There was no significant difference in lymphocyte infiltration among the patient groups and lymphocytes were present in much lower numbers than neutrophils; 3) Monocytes/macrophages were found in fat tissue but not in vessels. We speculate that neutrophils are the class of leukocytes that cause the majority of vascular cell dysfunction in preeclamptic women.

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“…We used arachidonic acid to activate the neutrophils because it is a physiologic activator and levels of arachidonic acid are elevated in women with preeclampsia10, 11. Previously, we provided evidence that COX-2 mediates neutrophil production of thromboxane, superoxide and TNFα19, 20. Here we show that COX-2 also mediates production of IL-8.…”

Section: Discussionmentioning

confidence: 54%

Neutrophil Expression of Cyclooxygenase 2 in Preeclampsia

2010

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The objective of this study was to determine: 1) if neutrophils of preeclamptic women express cyclooxygenase-2 (COX-2), and 2) if COX-2 mediates neutrophil interleukin-8 (IL-8) production. Neutrophils were isolated from heparinized blood collected from women with preeclampsia and normal pregnancy, and from normal nonpregnant women. COX-2 protein was measured in the neutrophils of the three groups by specific ELISA. To study the role of COX-2 in IL-8 production, neutrophils of normal pregnant women were activated with arachidonic acid and incubated overnight in Medium 199 with and without NS398, a specific COX-2 inhibitor. We found that neutrophils from preeclamptic women expressed significantly more COX-2 than neutrophils from normal pregnant or normal nonpregnant women. Arachidonic acid activated neutrophils to produce IL-8 which was completely inhibited by NS398. These data demonstrate that COX-2 is expressed in neutrophils of preeclamptic women and that COX-2 mediates IL-8 production by activated neutrophils.

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Neutrophils from pregnant women produce thromboxane and tumor necrosis factor-α in response to linoleic acid and oxidative stress

Cited by 31 publications

References 21 publications

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Neutrophils, but Not Lymphocytes or Monocytes, Infiltrate Maternal Systemic Vasculature in Women with Preeclampsia

Neutrophil Expression of Cyclooxygenase 2 in Preeclampsia

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