scholarly journals Fermented Chinese Formula Shuan-Tong-Ling Protects Brain Microvascular Endothelial Cells against Oxidative Stress Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Lingjing Tan ◽  
Xiang Zhang ◽  
Zhigang Mei ◽  
Jinfeng Wang ◽  
Xiaoli Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Endothelial Cells ◽  
Cell Senescence ◽  
Microvascular Endothelial Cells ◽  
Dependent Manner ◽  
Brain Microvascular Endothelial Cells ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Microvascular Endothelial

Fermented Chinese formulaShuan-Tong-Ling(STL), composed of fourteen medicinal herbs, was an experiential formula by Dr. Zhigang Mei for treating vascular encephalopathy, but the underlying mechanisms remained unknown. In this study, we aimed to investigate the protective effects of fermented STL on hydrogen peroxide- (H2O2-) induced injury in rat brain microvascular endothelial cells (BMECs) and the possible mechanisms. Cultured BMECs were treated with H2O2, STL, or nicotinamide (NAM, a SIRT1 inhibitor). Then, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was employed to detect cell proliferation and senescence-associated beta-galactosidase (SA-β-gal) was used to examine cell senescence. Cell nuclei were observed by 4′,6-diamidino-2-phenylindole. Additionally, changes in reactive oxygen species (ROS), superoxide dismutase (SOD), and glutathione (GSH) levels were measured. Expression of SIRT1, p21, and PGC-1αwas determined by western blot. Cell proliferation significantly increased with STL treatment in a dose-dependent manner. H2O2treatment could intensify cell senescence and nuclei splitting or pyknosis. With STL treatment, the reduced ROS level was accompanied by increased SOD and GSH activity. Further assays showed upregulation of SIRT1 and PGC-1αand downregulation of p21 after STL treatment. The results revealed that STL could protect BMECs against oxidative stress injury at least partially through the SIRT1 pathway.

HIV-1 Tat Mediated Effects on Focal Adhesion Assembly and Permeability in Brain Microvascular Endothelial Cells.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3105-3105
Author(s):  
Shalom Avraham ◽  
Shuxian Jiang ◽  
Tae-Hee Lee ◽  
O. Prakash ◽  
Hava Karsenty Avraham
Keyword(s):  
Endothelial Cells ◽  
Focal Adhesion ◽  
Microvascular Endothelial Cells ◽  
Mutant Form ◽  
Dependent Manner ◽  
Brain Microvascular Endothelial Cells ◽  
Adhesion Sites ◽  
Permeability Changes ◽  
Microvascular Endothelial ◽  
Hiv 1

Abstract The blood-brain barrier (BBB) is a network formed mainly by brain microvascular endothelial cells. The integrity of the BBB is critical for brain function. Breakdown of the BBB is commonly seen in AIDS patients with HIV-1-associated dementia (HAD), despite the lack of productive HIV-infection of the brain endothelium. The processes by which HIV causes these pathological conditions are not well understood. Here, we characterized the molecular mechanisms by which Tat mediates its pathogenic effects in-vitro on primary human brain microvascular endothelial cells (HBMECs). Tat treatment of HBMECs stimulated cytoskeletal organization and increased focal adhesion sites as compared to control cells or cells treated with heat-inactivated Tat. Pretreatment with Tat antibodies or with the specific inhibitor SU-1498, which interferes with VEGFR-2 (Flk-1/KDR) receptor phosphorylation, blocked the ability of Tat to stimulate focal adhesion assembly and the migration of HBMECs. Focal adhesion kinase (FAK) was tyrosine-phosphorylated by Tat and found to be an important component of focal adhesion sites. Inhibition of FAK by the dominant-interfering mutant form FRNK (FAK-related non-kinase) significantly blocked HBMEC migration and disrupted focal adhesions upon Tat activation. Furthermore, HIV-Tat induced permeability changes in HBMECs in a time dependent manner. Tat also impaired BBB permeability as observed in HIV-1 Tat transgenic mice. These studies define a mechanism for HIV-1 Tat in focal adhesion complex assembly in HBMECs, via activation of FAK, leading to cytoskeletal reorganization and permeability changes.

scholarly journals Hcp Family Proteins Secreted via the Type VI Secretion System Coordinately Regulate Escherichia coli K1 Interaction with Human Brain Microvascular Endothelial Cells

2011 ◽  
Vol 80 (3) ◽  
pp. 1243-1251 ◽  
Author(s):  
Yan Zhou ◽  
Jing Tao ◽  
Hao Yu ◽  
Jinjing Ni ◽  
Lingbing Zeng ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Human Brain ◽  
Microvascular Endothelial Cells ◽  
Dependent Manner ◽  
Brain Microvascular Endothelial Cells ◽  
Content Type ◽  
E Coli ◽  
Type Vi Secretion ◽  
Microvascular Endothelial ◽  
Cytoskeleton Rearrangement

Type VI secretion systems (T6SSs) are involved in the pathogenicity of several Gram-negative bacteria. Based on sequence analysis, we found that a cluster ofEscherichia colivirulencefactors (EVF) encoding a putative T6SS exists in the genome of the meningitis-causingE. coliK1 strain RS218. The T6SS-associated deletion mutants exhibited significant defects in binding to and invasion of human brain microvascular endothelial cells (HBMEC) compared with the parent strain. Hcp family proteins (the hallmark of T6SS), including Hcp1 and Hcp2, were localized in the bacterial outer membrane, but the involvements of Hcp1 and Hcp2 have been shown to differ inE. coli-HBMEC interaction. The deletion mutant ofhcp2showed defects in the bacterial binding to and invasion of HBMEC, while Hcp1 was secreted in a T6SS-dependent manner and induced actin cytoskeleton rearrangement, apoptosis, and the release of interleukin-6 (IL-6) and IL-8 in HBMEC. These findings demonstrate that the T6SS is functional inE. coliK1, and two Hcp family proteins participate in different steps ofE. coliinteraction with HBMEC in a coordinate manner, e.g., binding to and invasion of HBMEC, the cytokine and chemokine release followed by cytoskeleton rearrangement, and apoptosis in HBMEC. This is the first demonstration of the role of T6SS in meningitis-causingE. coliK1, and T6SS-associated Hcp family proteins are likely to contribute to the pathogenesis ofE. colimeningitis.

OxLDL Inhibits Brain Angiogenesis in Dose Dependent Manner via Reducing Level of VEGF and Angiopoietin-2: A Comprehensive Study

2017 ◽  
Author(s):  
Tasneem Alniqrish ◽  
Saed Khawaldeh
Keyword(s):  
Endothelial Cells ◽  
Human Brain ◽  
Angiogenic Factor ◽  
Microvascular Endothelial Cells ◽  
Dependent Manner ◽  
Brain Microvascular Endothelial Cells ◽  
Wide Range ◽  
Microvascular Endothelial ◽  
Dose Dependent ◽  
Brain Angiogenesis

Hyperlipidemia is recognized as a major health problem worldwide, moreover, it is considered as a major risk factor for cardiovascular and cerebrovascular diseases development. Since the majority of studies were performed to investigate the effect of hyperlipidemia on the angiogenesis of peripheral derived endothelial cell, this study aims to assess the effect of hyperlipidemia on the angiogenic response of human brain cells in a fast, easy and inexpensive method. Furthermore, it aims also to assess the involvement of Vascular Endothelial Growth Factor (VEGF) and angiopoietin. To achieve this aim, human Brain Microvascular Endothelial Cells (hBMECs) were treated with different concentration of Oxidized Low Density Lipoprotein (OxLDL) (1-100 μg/ml) for 24 hours. Migration rate and tube formation as markers of angiogenesis were performed, also Coomassie blue was used to detect protein level. OxLDL was found to inhibit brain angiogenesis in dose dependent manner over a wide range of concentrations (1-100 μg/ml). Using 1 μg/ml of OxLDL made minimum reduction of 10% whereas using 100 μg/ml of OxLDL resulted 70-80% reduction in the angiogenic potential of hBMECs within 24 hours. Moreover, OxLDL mediated its effect through reduced VEGF level and this effect was partially reversed by administered 5 ng/ml of VEGF. Additionally, OxLDL reduced the level of angiopoitin-2. This further supports the assumption that OxLDL has an anti-angiogenic effect in hBMECs and surely in the brain also. As a conclusion, OxLDL inhibits brain angiogenesis in dose dependent manner through reducing the level of angiogenic factor in human brain microvascular endothelial cells. We achieved our goal of having a preliminary indicator of brain angiogenesis under hyperlipidemia by using a simple but well-developed technique that incorporated the minimal number of tests and the cheapest.

Reaktion der Endothelzellen auf kurzzeitig physiologisch erhöhte hydrostatische Drücke und oxidativen Stress in vitro

2018 ◽  
Vol 236 (09) ◽  
pp. 1122-1128
Author(s):  
Carolina Mann ◽  
Solon Thanos ◽  
Katrin Brockhaus ◽  
Franz H. Grus ◽  
Norbert Pfeiffer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endotheliale Dysfunktion ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Microvascular Endothelial

Zusammenfassung Hintergrund Im Rahmen der Pathogenese des Glaukoms wird die endotheliale Dysfunktion zunehmend diskutiert. Peripapilläre Blutungen sind diagnostisch wegweisend. Die Korrelation von Glaukomerkrankungen mit vaskulärem Dysregulationssyndrom ist eindeutig. Ziel dieser Studie ist es, die genaue Reaktion der Endothelzellen auf erhöhten hydrostatischen und oxidativen Stress zu untersuchen. Material und Methoden In vitro wurden primär dissoziierte BMECs (brain microvascular endothelial cells) für 3 Tage normalem und leicht erhöhtem hydrostatischem Druck von 60 und 120 mmHg in einer Druckkammer ausgesetzt. Zusätzlich wurden sowohl druckbelastete als auch nicht druckbelastete Zellen oxidativem Stress in Form von geringen Konzentrationen H2O2 ausgesetzt. Ein Live/Dead Assay wurde durchgeführt, um die Zellviabilität zu messen. Morphologisch wurden die Zellen mit immunhistochemischer Aktinfärbung beurteilt. Ergebnisse Interessanterweise zeigten die Endothelzellen sowohl unter 60 mmHg als auch unter 120 mmHg kein vermehrtes Absterben im Vergleich zu den Zellen ohne Belastung. Auch morphologisch zeigten sich keine großen Unterschiede. Gegenüber oxidativem Stress wurden alle Zellen schon bei kleinen Mengen geschädigt. Keinen Unterschied konnte man zwischen oxidativem Stress ohne vorherige Druckbelastung und oxidativem Stress mit vorheriger Druckbelastung von 120 mmHg für 3 Tage feststellen. Schlussfolgerung Wir konnten keinen direkten Effekt in Form von vermehrtem Zelluntergang der Endothelzellen auf erhöhten hydrostatischen Druck feststellen. Allerdings zeigt die Reaktion auf die geringen Konzentrationen von oxidativem Stress, dass die Zellen im Rahmen der Pathogenese des Glaukoms doch in Mitleidenschaft gezogen werden. Der oxidative Stress scheint hier eine besondere Rolle zu spielen.

scholarly journals Integrin α4β1/VCAM-1 Interaction Evokes Dynamic Cell Aggregation Between Immune Cells and Human Lung Microvascular Endothelial Cells at Infectious Hemolysis

2021 ◽  
Vol 12 ◽  
Author(s):  
Hai-Yan Lou ◽  
Hai-Peng Yan ◽  
Long-Gui Yang ◽  
Jiang-hua Fan ◽  
William C. Cho ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
T Cell ◽  
Immune Cells ◽  
Human Lung ◽  
Cell Aggregation ◽  
Microvascular Endothelial Cells ◽  
T Cell Proliferation ◽  
Dependent Manner ◽  
Microvascular Endothelial

Bacterial and viral infection is a common cause of pneumonia, respiratory failure, and even acute respiratory distress syndrome. Increasing evidence indicates that red blood cells (RBCs) may contribute to immune response and inflammation. However, the precise molecular mechanisms that link RBC and hemolysis to the development and progression of inflammatory pathologies are not entirely understood. In this study, we used bacterial endotoxin, lipopolysaccharide (LPS), to mimic an infectious hemolysis and found that RBCs dynamically regulated cell aggregation between immune cells and human lung microvascular endothelial cells (HLMVEC). When RBCs were treated with LPS, integrin α4β1 was increased and was accompanied by cytokines and chemokines release (TNF-α, IL-1β, IL-6, IL-8, IFN-γ, CXCL12, CCL5, CCL7 and CCL4). Upon α4β1 elevation, RBCs not only facilitated mature monocyte derived dendritic cell (mo-DCs) adhesion but also promoted HLMVEC aggregation. Furthermore, co-culture of the supernatant of LPS pre-treated RBCs with mo-DCs could promote naïve CD4 T cell proliferation. Notably, the filtered culture from LPS-lysed RBCs further promoted mo-DCs migration in a concentration dependent manner. From a therapeutic perspective, cyclic peptide inhibitor of integrin α4β1 combined with methylprednisolone (α4β1/Methrol) remarkably blocked RBCs aggregation to mo-DCs, HLMVEC, or mo-DCs and HLMVEC mixture. Moreover, α4β1/Methrol dramatically reduced mo-DCs migration up-regulated glucocorticoid-induced leucine zipper in mo-DCs, and ultimately reversed immune cell dysfunction induced by hemolysis. Taken together, these results indicate that integrin α4β1 on RBCs could mediate cell-cell interaction for adaptive immunity through influencing cell adhesion, migration, and T cell proliferation.

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