Increased neutrophil-endothelial adhesion induced by placental factors is mediated by platelet-activating factor in preeclampsia

Wang, Yuping; Adair, David; Weeks, Jonathan W.; Lewis, David F.; Alexander, Steven

doi:10.1016/s1071-5576(99)00004-0

Cited by 26 publications

(31 citation statements)

References 26 publications

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“…However, some insights into the possible identity of these factors are provided by previously published work. For example, it has been shown that the increased neutrophil-endothelial adhesion induced by placental factors is mediated by platelet-activating factor (10). Endothelial protease-activated receptors, protease thrombin, and trypsin have also been implicated in the endothelial dysfunction induced by placental factors (12).…”

Section: Discussionmentioning

confidence: 99%

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Placental Trophoblast-Derived Factors Diminish Endothelial Barrier Function

Wang¹,

Lewis²,

Gu³

et al. 2004

The Journal of Clinical Endocrinology & Metabolism

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Although increased vascular permeability is an important event in the pathogenesis of preeclampsia, the origin of the circulating factor(s) that elicits this endothelial barrier dysfunction is not known. In this study, we use coculture of endothelial cells and placental trophoblast cells to determine whether placental trophoblasts are a potential source of the factor(s) that mediate the increased vascular permeability of preeclampsia. Human umbilical vein endothelial cells grown in Transwell inserts or on coverslips were cocultured with trophoblast cells isolated from normal and preeclamptic placentas or placenta conditioned media. Endothelial cell barrier function was determined by: 1). measurements of electrical resistance and leakage of horseradish peroxidase, and 2). immunofluorescent staining of vascular endothelial-cadherin, pan-cadherin, and occludin. Uterine myometrium endothelial cells were also studied for comparison. We observed the following: 1). electrical resistance was significantly (P < 0.01) decreased (compared with control endothelial cells) in endothelial cell monolayers cocultured with normal trophoblast cells and further reduced in endothelial cells cocultured with preeclamptic trophoblast cells; 2). an increased horseradish peroxidase leakage that was correlated with the decreased electrical resistance in cocultured cells; and 3). disorganized tight junction proteins and an altered distribution of vascular endothelial-cadherin and occludin in monolayers of endothelial cells cocultured with preeclamptic trophoblast cells. Similar responses were noted in uterine myometrium endothelial cells. We conclude that: 1). placental trophoblast cells produce factors that diminish the barrier function of endothelial cells; 2). endothelial tight junctions are more susceptible to factors released from preeclamptic trophoblast cells than from normal trophoblast cells; and 3). these results implicate trophoblast-derived factors in the increased vascular permeability associated with preeclampsia.

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Section: Discussionmentioning

confidence: 99%

“…Placental conditioned medium was prepared as follows (10,12). Briefly, fresh placentas from normal and preeclamptic pregnancies were collected and processed immediately after delivery.…”

Section: Coculture Of Endothelial Cells With Trophoblastsmentioning

confidence: 99%

Placental Trophoblast-Derived Factors Diminish Endothelial Barrier Function

Wang¹,

Lewis²,

Gu³

et al. 2004

The Journal of Clinical Endocrinology & Metabolism

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“…Preeclampsia is defined severe if one or more of the following criteria is present: maternal blood pressure ≥160/110 mmHg; proteinuria >3+ or >5 g/24 h; oliguria of less than 500 ml in 24 h; intrauterine growth restriction, and presence of persistent headache or visual disturbances. Preeclamptic placental conditioned medium was prepared as previously described [9,15,16]. Briefly, villous tissue, excluding basal plates and fetal membranes, was incubated with serum free Dulbecco's Modified Eagles Medium (DMEM, Sigma Chemical Inc., St Louis, MO) for 48 h. At the end of incubation, the culture medium was collected and stored at -70 °C until use.…”

Section: Preparation Of Placental Conditioned Mediummentioning

confidence: 99%

Contractility of Placental Vascular Smooth Muscle Cells in Response to Stimuli Produced by the Placenta: Roles of ACE vs. Non-ACE and AT1 vs. AT2 in Placental Vessel Cells

Benoit

Zhang

et al. 2008

Placenta

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Our previously published work has shown that non-ACE angiotensin II (Ang II) generating system is dominate in the placenta and may play a critical role in regulation of placental vascular contractile function. In the present study, using a collagen gel contraction assay we further studied contractility of placental vascular smooth muscle cells (VSMCs) in response to factors produced by preeclamptic (PE) placentas. Placental VSMCs/type-1 collagen gels were incubated with PE placental conditioned medium in the presence or absence of inhibitors or receptor blockers. Captopril (an ACE inhibitor), chymostatin (a non-ACE chymase inhibitor), losartan (an AT1 receptor blocker) and PD123,319 (an AT2 receptor blocker) were used to study the specific ACE vs. non-ACE and AT1 vs. AT2 effects on placental VSMC contractility, respectively. Our results showed that chymostatin, but not captopril, and PD123,319, but not losartan, significantly attenuated placental VSMC/collagen gel contraction, p < 0.01, respectively. The inhibitory effects of chymostatin and PD123,319 were dosedependent. Our results suggest that chymase, a non-ACE Ang II generating enzyme, may contribute significantly to Ang II generated in the placenta vascular tissue and that the AT2 receptor may play an important role in the regulation of Ang II induced contractility of placental VSMCs. These results provide new insights into Ang II generation and Ang II receptor regulation of vessel contractile function in the placental vasculature. These results also suggest the potential role of increased chymase activity and altered AT2 receptor function in placental related pregnancy disorders such as preeclampsia and IUGR.

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“…Placental conditioned media (CM) were prepared from villous tissue explant culture from the placentas of preeclamptic patients as previously described [29,30]. Briefly, placentas were obtained immediately after delivery from preeclamptic pregnancies.…”

Section: Conditioned Medium Preparationmentioning

confidence: 99%

Vasoreactivity of Chorionic Plate Arteries in Response to Vasoconstrictors Produced by Preeclamptic Placentas

2007

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Inadequate blood flow and increased vasoconstriction of the placenta contribute to pregnancy associated disorders such as preeclampsia (PE). Because placental vessels lack autonomic innervation, humoral effects of the placenta must play critical roles in regulation of fetal-placental vascular contractility. In this study, we examined the nature of humoral factors produced by PE trophoblasts on placental vessel contractility using an organ bath perfusion model. Vasomotor responses were studied in vitro using placental chorionic plate arteries. Vessel rings from third branch chorionic plate arteries were dissected from human placentas following normal or PE delivery. The arterial rings were equilibrated in Krebs Henseleit buffer and exposed to placental conditioned medium, which was prepared by culture of villous tissue from PE placentas. Receptor antagonists for angiotensin II (ANG II), thromboxane (TX), and endothelin (ET) were used to determine which humoral factor produced by placental tissue (trophoblasts) was more effective in promoting vasoconstriction. The role of angiotensin converting enzyme (ACE) and non-ACE ANG II generating enzymes in regulation of placental vasomotor tone were also investigated. A total of 80 arterial rings from 48 placentas were studied. Our results showed: 1) enhanced vasomotor tone in arteries from PE placentas compared to those from normal placentas; 2) PE-CM induced vaso-constrictive activity could be partially attenuated by receptor antagonists for TX, ANG II and ET, respectively; and 3) chymostatin (a chymase inhibitor) produced a stronger inhibitory effect than captopril (ACE inhibitor) on PE conditioned medium induced vasoconstriction. Our data demonstrate increased vasocontractility in PE placentas and suggest that the non-ACE pathway is probably a major source of ANG II produced in the human placenta.

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Increased neutrophil-endothelial adhesion induced by placental factors is mediated by platelet-activating factor in preeclampsia

Cited by 26 publications

References 26 publications

Placental Trophoblast-Derived Factors Diminish Endothelial Barrier Function

Placental Trophoblast-Derived Factors Diminish Endothelial Barrier Function

Contractility of Placental Vascular Smooth Muscle Cells in Response to Stimuli Produced by the Placenta: Roles of ACE vs. Non-ACE and AT1 vs. AT2 in Placental Vessel Cells

Vasoreactivity of Chorionic Plate Arteries in Response to Vasoconstrictors Produced by Preeclamptic Placentas

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