Mid trimester amniotic fluid soluble receptor tunica interna endothelial cell kinase-2 levels and risk for preeclampsia

AbstractObjectiveTo determine the concentrations of soluble endoglin (sCD105) and endothelial cell-specific molecule-1 (ESM-1) in the amniotic fluid (AF) of pregnant women, and to investigate the relationship between these concentrations and neural tube defects (NTDs).MethodsAF concentrations of sCD105 and ESM-1 were measured in the study group, which included 60 pregnant women complicated with NTDs, and 64 pregnant women with unaffected healthy fetuses (control group). The AF concentrations of sCD105 and ESM-1 in both groups were measured using enzyme-linked immunosorbent assay and compared.ResultsThere were no significant differences in terms of the mean AF concentrations of sCD105 and ESM-1 between the groups (P=0.141, P=0.084, respectively). There was a significant difference between the AF sCD105 concentrations in those with gestational age <24 weeks (n=101) and ≥24 weeks (n=23) (X̅<24=76.35±126.62 vs. X≥24=39.87±58.32, P=0.041). AF ESM-1 concentrations were found to be statistically significant in the gestational age <22 weeks (n=90) and ≥22 weeks (n=34) groups (X̅<22=135.91±19.26 vs. X̅≥22=148.56±46.85, P=0.035). A positive and low-level relation at a statistically significant level was determined between the gestational age and AF ESM-1 concentration in the study group (r=0.257; P=0.048).ConclusionAF concentrations of sCD105 and ESM-1 were not associated with the development of NTDs. Unlike studies that reported that ESM-1 concentrations decreased in maternal plasma with increased gestational age, we determined an increase that was proportionate to gestational age in AF.

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An Ultrastructural Study of Pericytes

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010010007x ◽

1968 ◽

Vol 26 ◽

pp. 66-67

Author(s):

T. M. Murad ◽

E. von Haam

Keyword(s):

Plasma Membrane ◽

Endothelial Cell ◽

Basement Membrane ◽

Blood Vessel ◽

Vascular Endothelial Cells ◽

Myoepithelial Cells ◽

Capillary Blood ◽

The Body ◽

Capillary Blood Vessel ◽

Outer Plasma Membrane

Pericytes are vascular satellites present around capillary blood vessels and small venules. They have been observed in almost every tissue of the body and are thought to be related to vascular smooth muscle cells. Morphologically pericytes have great similarity to vascular endothelial cells and also slightly resemble myoepithelial cells.The present study describes the ultrastructural morphology of pericytes in normal breast tissue and in benign tumor of the breast. The study showed that pericytes are ovoid or elongated cells separated from the endothelial cell of the capillary blood vessel by the basement membrane of endothelial cell. The nuclei of pericytes are often very distinctive. Although some are round, oval, or elongated, others show marked irregularity and infolding of the nuclear membrane. The cytoplasm shows mono-or bipolar extension in which the cytoplasmic organelles are located (Fig. 1). These cytoplasmic extensions embrace the capillary blood vessel incompletely. The plasma membrane exhibits multiple areas of focal condensation called hemidesmosomes (Fig. 2, arrow). A variable number of pinocytotic vesicles are frequently seen lining the outer plasma membrane. Normally pericytes are surrounded by a basement membrane which is found more consistently on the outer plasma membrane separating the pericytes from the stromal connective tissue.

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Effect of angiotensin(1-7) on the expression of E-selectin induced by angiotensinII and its mechanism in vascular endothelial cell

Cell Biology International ◽

10.1042/cbi034s071a ◽

2010 ◽

Vol 34 (8) ◽

pp. S71-S71

Author(s):

Xiaohui Shen ◽

Zhi‑Bin Wen ◽

Na Li ◽

Qingmei Cheng ◽

Xiaofan He ◽

...

Keyword(s):

Endothelial Cell ◽

Vascular Endothelial Cell ◽

Vascular Endothelial

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Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

Clinical Science ◽

10.1042/cs20190514 ◽

2019 ◽

Vol 133 (20) ◽

pp. 2045-2059 ◽

Cited By ~ 4

Author(s):

Da Zhang ◽

Xiuli Wang ◽

Siyao Chen ◽

Selena Chen ◽

Wen Yu ◽

...

Keyword(s):

Hydrogen Sulfide ◽

Endothelial Cell ◽

Pulmonary Artery ◽

Cell Model ◽

Site Directed Mutagenesis ◽

Critical Event ◽

Hypertensive Rats ◽

Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

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