Preeclampsia Does Not Alter Vascular Growth and Expression of CD31 and Vascular Endothelial Cadherin in Human Placentas

Li, Yan; Zhao, Yingjie; Zou, Qingyun; Zhang, Kevin; Wu, Yanming; Zhou, Chi; Wang, Kai; Zheng, Jing

doi:10.1369/0022155414558063

Cited by 25 publications

(19 citation statements)

References 48 publications

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“…Despite the significant overexpression of endoglin (CD105) that is expected to be correlated with angiogenesis, in the present study we found MVD in PE to be comparable to control group. Similarly were the results reported by Li et al, (2015) [30] .…”

Section: Similar To Our Results Sankar Et Al (2012) Andsupporting

confidence: 89%

Placenta Of Late Onset Preeclampsia Without Fetal Growth Restriction : Is It Different From The Normal?

Wageh

Nagib

Eid

2019

Evidence Based Women's Health Journal

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Background: Preeclampsia (PE) is one of the most common pregnancy complications affecting approximately 5-7% of pregnant women worldwide. Pathogenesis of PE is still mysterious. Literature studies reported differences between early and late onset PE. Also, whether placenta of late-onset PE without fetal growth restriction (FGR) is different from normal one needs further declaration. Objective: This study aims at evaluating the placental microvessel density (MVD), apoptosis and endoglin (CD105) expression in late-onset PE without FGR. Patients and Methods: Placentae of 15 PE and 15 matched control ones were evaluated grossly, microscopically and by immunohistochemistry for caspase-3, CD 34 and CD105. Results: Placentas in PE group showed a statistically significant difference as regard size, syncytial knots, perivillous fibrin deposition, villous infarction increased apoptosis, and endoglin (CD105) expression. However, the percentage of terminal villi and microvessel density (MVD) were comparable in both groups. Conclusion: Placenta from late onset PE without FGR is still different from the normal placenta whatever time onset of PE pathogenesis may be similar. Absence of changes in MVD may explain good fetal outcome.

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Section: Similar To Our Results Sankar Et Al (2012) Andsupporting

confidence: 89%

Placenta Of Late Onset Preeclampsia Without Fetal Growth Restriction : Is It Different From The Normal?

Wageh

Nagib

Eid

2019

Evidence Based Women's Health Journal

View full text Add to dashboard Cite

show abstract

“…In an arterial pathology such as preeclampsia, CD31 immunoreactivity is lower in the placenta than in control pregnancies [24,26]. However, Li et al [27] showed no significant differences in CD31 level in the placenta of women with preeclampsia. In general, angiogenesis and lymphangiogenesis are modified in vascular pathology [28].…”

Section: Discussionmentioning

confidence: 96%

Increased Angiogenesis and Lymphangiogenesis in the Placental Villi of Women with Chronic Venous Disease during Pregnancy

Ortega

Sáez

Fraile-Martínez

et al. 2020

IJMS

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Pregnancy is a period in a woman’s life associated with an increased risk of developing lower extremity chronic venous disease (CVD). Pregnancy-associated CVD is associated with changes in placental villi. We investigated angiogenesis and lymphangiogenesis in the placental villi of women with CVD during pregnancy compared with healthy controls with no history of CVD (HC). An observational, analytical, and prospective cohort study was conducted on 114 women in their third trimester of pregnancy (32 weeks). Sixty-two participants were clinically diagnosed with CVD. In parallel, 52 controls with no history of CVD (HC) were studied. Gene and protein expression of CD31, podoplanin (D2-40), Flt-1, and placental growth factor (PIGF) was analysed by real-time polymerase chain reaction (RT-qPCR) and immunohistochemistry. CD31 and D2-40 gene expression was significantly greater in the placental villi of women with CVD, as were the numbers of vessels positive for CD31 and D2-40. Significantly higher gene and protein expression of Flt-1 and PIGF was observed in the placental villi of women with CVD. Histological analysis showed more placental villi with periodic acid of Schiff (PAS)-positive material in women with CVD. Our results show a connection between pregnancy-associated CVD and leading to higher proangiogenic and lymphangiogenic activity in placental villi.

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“…[12,14,22,25] A single dose of ITE (20 µM) rapidly decreased ( p < 0.05) AhR protein levels in HPAEC by 55.9, 72.2, 70.6, 74.6, and 59.8% on 1, 8, 16, 24, and 48 hr, respectively (Fig. 5A).…”

Section: Resultsmentioning

confidence: 99%

“…Immunolocalization of AhR was visualized by indirect detection via the avidin: biotinylated-peroxidase complex method (Vector Laboratories, Burlingame, CA) as described. [23–25] Briefly, after deparaffinized and dehydrated, the microarray was boiled in a 10 mM citrate buffer solution (pH 6.0) in a microwave for 10 min for antigen retrieval. Endogenous peroxidase activity was quenched using 3% H 2 O 2 .…”

Section: Methodsmentioning

confidence: 99%

ITE inhibits growth of human pulmonary artery endothelial cells

Pang

Zou

et al. 2017

Experimental Lung Research

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Aim Pulmonary arterial hypertension (PAH), a deadly disorder is associated with excessive growth of human pulmonary artery endothelial (HPAECs) and smooth muscle (HPASMCs) cells. Current therapies primarily aim at promoting vasodilation, which only ameliorates clinical symptoms without a cure. 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) is an endogenous aryl hydrocarbon receptor (AhR) ligand, and mediates many cellular function including cell growth. However, the roles of ITE in human lung endothelial cells remain elusive. Herein, we tested a hypothesis that ITE inhibits growth of human pulmonary artery endothelial cells via AhR. Materials and Methods Immunohistochemistry was performed to localize AhR expression in human lung tissues. The crystal violet method and MTT assay were used to determine ITE’s effects on growth of HPAECs. The AhR activation in HPAECs was confirmed using Western blotting and RT-qPCR. The role of AhR in ITE-affected proliferation of HPAECs was assessed using siRNA knockdown method followed by the crystal violet method. Results Immunohistochemistry revealed that AhR was present in human lung tissues, primarily in endothelial and smooth muscle cells of pulmonary veins and arteries, as well as in bronchial and alveolar sac epithelia. We also found that ITE dose- and time-dependently inhibited proliferation of HPAECs with a maximum inhibition of 83% at 20 µM after 6 days of treatment. ITE rapidly decreased AhR protein levels, while it increased mRNA levels of cytochrome P450 (CYP), family 1, member A1 (CYP1A1) and B1 (CYP1B1), indicating activation of the AhR/CYP1A1 and AhR/CYP1B1 pathways in HPAECs. The AhR siRNA significantly suppressed AhR protein expression, whereas it did not significantly alter ITE-inhibited growth of HPAECs. Conclusions ITE suppresses growth of HPAECs independent of AhR, suggesting that ITE may play an important role in preventing excessive growth of lung endothelial cells.

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Preeclampsia Does Not Alter Vascular Growth and Expression of CD31 and Vascular Endothelial Cadherin in Human Placentas

Cited by 25 publications

References 48 publications

Placenta Of Late Onset Preeclampsia Without Fetal Growth Restriction : Is It Different From The Normal?

Placenta Of Late Onset Preeclampsia Without Fetal Growth Restriction : Is It Different From The Normal?

Increased Angiogenesis and Lymphangiogenesis in the Placental Villi of Women with Chronic Venous Disease during Pregnancy

ITE inhibits growth of human pulmonary artery endothelial cells

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