Microvascular endothelial cell activation is present in the umbilical placental microcirculation in fetal placental vascular disease

2004 ◽  
Vol 190 (3) ◽  
pp. 596-601 ◽  
Author(s):  
Xin Wang ◽  
Neil Athayde ◽  
Brian Trudinger
Keyword(s):  
Endothelial Cell ◽  
Vascular Disease ◽  
Cell Activation ◽  
Microvascular Endothelial Cell ◽  
Endothelial Cell Activation ◽  
Microvascular Endothelial

scholarly journals Brucella abortus-Stimulated Platelets Activate Brain Microvascular Endothelial Cells Increasing Cell Transmigration through the Erk1/2 Pathway

Pathogens ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 708
Author(s):  
Ana María Rodríguez ◽  
Aldana Trotta ◽  
Agustina P. Melnyczajko ◽  
M. Cruz Miraglia ◽  
Kwang Sik Kim ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Brucella Abortus ◽  
Cell Activation ◽  
Transendothelial Migration ◽  
Endothelial Activation ◽  
Microvascular Endothelial Cell ◽  
Inflammatory Disorder ◽  
Endothelial Cell Activation ◽  
Microvascular Endothelial

Central nervous system invasion by bacteria of the genus Brucella results in an inflammatory disorder called neurobrucellosis. A common feature associated with this pathology is blood–brain barrier (BBB) activation. However, the underlying mechanisms involved with such BBB activation remain unknown. The aim of this work was to investigate the role of Brucella abortus-stimulated platelets on human brain microvascular endothelial cell (HBMEC) activation. Platelets enhanced HBMEC activation in response to B. abortus infection. Furthermore, supernatants from B. abortus-stimulated platelets also activated brain endothelial cells, inducing increased secretion of IL-6, IL-8, CCL-2 as well as ICAM-1 and CD40 upregulation on HBMEC compared with supernatants from unstimulated platelets. Outer membrane protein 19, a B. abortus lipoprotein, recapitulated B. abortus-mediated activation of HBMECs by platelets. In addition, supernatants from B. abortus-activated platelets promoted transendothelial migration of neutrophils and monocytes. Finally, using a pharmacological inhibitor, we demonstrated that the Erk1/2 pathway is involved in the endothelial activation induced by B. abortus-stimulated platelets and also in transendothelial migration of neutrophils. These results describe a mechanism whereby B. abortus-stimulated platelets induce endothelial cell activation, promoting neutrophils and monocytes to traverse the BBB probably contributing to the inflammatory pathology of neurobrucellosis.

[P4-118]: HIGH-DENSITY LIPOPROTEINS SUPPRESS Aβ-INDUCED BRAIN MICROVASCULAR ENDOTHELIAL CELL ACTIVATION

2017 ◽  
Vol 13 (7S_Part_27) ◽  
pp. P1302-P1302
Author(s):  
Emily B. Button ◽  
Jerome Robert ◽  
Sophie Stukas ◽  
Guilaine Boyce ◽  
Ebrima Gibbs ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Activation ◽  
High Density ◽  
High Density Lipoproteins ◽  
Microvascular Endothelial Cell ◽  
Brain Microvascular Endothelial Cell ◽  
Endothelial Cell Activation ◽  
Microvascular Endothelial

Adiponectin Diminishes Organ-Specific Microvascular Endothelial Cell Activation Associated With Sepsis

Shock ◽  
2012 ◽  
Vol 37 (4) ◽  
pp. 392-398 ◽  
Author(s):  
Matijs van Meurs ◽  
Pedro Castro ◽  
Nathan I. Shapiro ◽  
Shulin Lu ◽  
Midori Yano ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Activation ◽  
Microvascular Endothelial Cell ◽  
Endothelial Cell Activation ◽  
Organ Specific ◽  
Microvascular Endothelial

Functional analyses reveal the greater potency of preadipocytes compared with adipocytes as endothelial cell activator under normoxia, hypoxia, and TNFα exposure

2009 ◽  
Vol 297 (3) ◽  
pp. E735-E748 ◽  
Author(s):  
Isabelle Mack ◽  
Rachida S. BelAiba ◽  
Talija Djordjevic ◽  
Agnes Görlach ◽  
Hans Hauner ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Cell Activation ◽  
Microvascular Endothelial Cell ◽  
Low Grade ◽  
Monocyte Adhesion ◽  
Endothelial Cell Activation ◽  
Sgbs Cells ◽  
Stimulation Of ◽  
Cell Cell

Obesity is associated with a state of chronic low-grade inflammation. Immune cells accumulate in white adipose tissue (WAT). The vascular endothelium plays an interactive role in these infiltration and inflammatory processes. Mature and hypertrophic adipocytes are considered as the major adipogenic cell type secreting proinflammatory cytokines in WAT. In contrast, the proinflammatory capacity of preadipocytes and their role in endothelial cell activation have been neglected so far. To gain new insights into this molecular and cellular cross-talk, we examined the proinflammatory expression and secretion of normoxia, hypoxia, and TNFα-treated human preadipocytes and adipocytes (SGBS cells) and their impact on human microvascular endothelial cell (HMEC-1) function. In this study, stimulation of HMEC-1 with conditioned media (CM) from preadipocytes increased endothelial ICAM-1 expression and monocyte adhesion but not adipocyte-CM. After hypoxia and TNFα stimulation of SGBS cells, adipocyte-CM induced and preadipocyte-CM enhanced the monocyte adhesion. Concordantly, the expression of proinflammatory adipokines was considerably higher in preadipocytes than in adipocytes. SGBS-CM upregulated the phosphorylation of three MAPK pathways, STAT1/3, and c-Jun in HMEC-1, whereas the NF-κB pathway was not affected. Inhibitor experiments showed that monocyte/endothelial cell-cell adhesion and endothelial ICAM-1 expression was JNK and JAK-1/STAT1/3 pathway dependent and revealed IL-6 as a major mediator in CM increasing monocyte/endothelial cell-cell adhesion via the STAT1/3 pathway. Our study shows that preadipocytes rather than adipocytes operate as potent activators of endothelial cells. This can be enhanced in preadipocytes and induced in adipocytes by TNFα and hypoxia in a manner similar to what may occur in WAT in the etiology of obesity.

scholarly journals Glutathione Peroxidase-1 Deficiency Augments Proinflammatory Cytokine-induced Redox Signaling and Human Endothelial Cell Activation

2011 ◽  
Vol 286 (41) ◽  
pp. 35407-35417 ◽  
Author(s):  
Edith Lubos ◽  
Neil J. Kelly ◽  
Scott R. Oldebeken ◽  
Jane A. Leopold ◽  
Ying-Yi Zhang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Glutathione Peroxidase ◽  
Adhesion Molecule ◽  
Cell Activation ◽  
Microvascular Endothelial Cells ◽  
Endothelial Cell Activation ◽  
Glutathione Peroxidase 1 ◽  
Tnf Α ◽  
Microvascular Endothelial

Glutathione peroxidase-1 (GPx-1) is a crucial antioxidant enzyme, the deficiency of which promotes atherogenesis. Accordingly, we examined the mechanisms by which GPx-1 deficiency enhances endothelial cell activation and inflammation. In human microvascular endothelial cells, we found that GPx-1 deficiency augments intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression by redox-dependent mechanisms that involve NFκB. Suppression of GPx-1 enhanced TNF-α-induced ROS production and ICAM-1 expression, whereas overexpression of GPx-1 attenuated these TNF-α-mediated responses. GPx-1 deficiency prolonged TNF-α-induced IκBα degradation and activation of ERK1/2 and JNK. JNK or NFκB inhibition attenuated TNF-α induction of ICAM-1 and VCAM-1 expression in GPx-1-deficient and control cells, whereas ERK1/2 inhibition attenuated only VCAM-1 expression. To analyze further signaling pathways involved in GPx-1-mediated protection from TNF-α-induced ROS, we performed microarray analysis of human microvascular endothelial cells treated with TNF-α in the presence and absence of GPx-1. Among the genes whose expression changed significantly, dual specificity phosphatase 4 (DUSP4), encoding an antagonist of MAPK signaling, was down-regulated by GPx-1 suppression. Targeted DUSP4 knockdown enhanced TNF-α-mediated ERK1/2 pathway activation and resulted in increased adhesion molecule expression, indicating that GPx-1 deficiency may augment TNF-α-mediated events, in part, by regulating DUSP4.

Sign in / Sign up

Export Citation Format

Share Document