Modulation of the Vascular Endothelium during Infection - The Role of NF-κB Activation

2002 ◽  
pp. 86-105 ◽  
Author(s):  
A. Bierhaus ◽  
P.P. Nawroth
Keyword(s):  
Vascular Endothelium ◽  
Nf Kappa B

scholarly journals Reduced Flow-Mediated Dilatation Is Not Related to COVID-19 Severity Three Months after Hospitalization for SARS-CoV-2 Infection

2021 ◽  
Vol 10 (6) ◽  
pp. 1318
Author(s):  
Marianne Riou ◽  
Walid Oulehri ◽  
Cedric Momas ◽  
Olivier Rouyer ◽  
Fabienne Lebourg ◽  
...  
Keyword(s):  
Vascular Endothelium ◽  
Matched Control ◽  
Acute Infection ◽  
Critical Role ◽  
Lung Damage ◽  
Vascular Effect ◽  
Flow Mediated Dilatation ◽  
Artery Flow

The coronavirus disease 2019 (COVID-19) pandemic has spread rapidly worldwide, with more than two million deaths. Evidence indicates the critical role of the vascular endothelium in its pathophysiology but, like potential changes in functional vasodilation, the vascular effect of SARS-CoV-2 at a given distance from the acute infection is largely unknown. We assessed brachial artery flow-mediated dilatation (FMD) in 27 COVID-19 patients needing conventional or intensive care unit hospitalization, three months after SARS-CoV-2 infection diagnosis and in nine age- and sex- matched control subjects. Interestingly, the FMD was lower in COVID-19 patients as compared to controls (8.2 (7.2–8.9) vs. 10.3 (9.1–11.7)); p = 0.002, and half of the hospitalized COVID-19 survivors presented with a reduced FMD < 8% at three months of COVID-19 onset. Impaired FMD was not associated with severe or critical SARS-CoV-2 infection, reflected by ICU hospitalization, total hospitalization duration, or severity of lung damage. In conclusion, reduced FMD is often observed even three months after hospitalization for SARS-CoV-2 infection, but such alteration predominantly appears to not be related to COVID-19 severity. Longer and larger follow-up studies will help to clarify the potential prognosis value of FMD among COVID-19 patients, as well as to further determine the mechanisms involved.

Role of Adhesion Molecules and Vascular Endothelium in the Pathogenesis of Sickle Cell Disease

Hematology ◽  
2007 ◽  
Vol 2007 (1) ◽  
pp. 84-90 ◽  
Author(s):  
Marilyn J. Telen
Keyword(s):  
Sickle Cell Disease ◽  
Red Blood Cells ◽  
Adhesion Molecules ◽  
Sickle Cell ◽  
Vascular Endothelium ◽  
Blood Cells ◽  
Cell Disease ◽  
Adhesive Interactions ◽  
Lines Of Evidence

AbstractA number of lines of evidence now support the hypothesis that vaso-occlusion and several of the sequelae of sickle cell disease (SCD) arise, at least in part, from adhesive interactions of sickle red blood cells, leukocytes, and the endothelium. Both experimental and genetic evidence provide support for the importance of these interactions. It is likely that future therapies for SCD might target one or more of these interactions.

The dual role of the contact system in bacterial infectious disease

2007 ◽  
Vol 98 (09) ◽  
pp. 497-502 ◽  
Author(s):  
Inga-Maria Frick ◽  
Lars Björck ◽  
Heiko Herwald
Keyword(s):  
Vascular Endothelium ◽  
Blood Cells ◽  
State Of The Art ◽  
Contact System ◽  
Intrinsic Pathway ◽  
Kinin System ◽  
Inflammatory Reactions ◽  
Bacterial Infectious Disease ◽  
Kallikrein Kinin System

SummaryHemostasis is a sensitive and tightly regulated process, involving the vascular endothelium and blood cells as well as factors of the coagulation and fibrinolytic cascades. Over the last four decades evidence has accumulated that during infection, inflammatory mediators from the microbe and/or host are capable to modulate the equilibrium between the procoagulant and anticoagulant status of the host. Dependent on the mode of activation, these changes can cause either local or systemic inflammatory reactions that may be beneficial or deleterious to the human host. The present review aims to present the state of the art with respect to the role of the contact system (also known as the intrinsic pathway of coagulation or the kallikrein/kinin system) in innate immunity and systemic inflammatory reactions.

scholarly journals Acute Myeloid and Lymphoblastic Leukemia Cell Interactions with Endothelial Selectins: Critical Role of PSGL-1, CD44 and CD43

Cancers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1253 ◽  
Author(s):  
Caroline Spertini ◽  
Bénédicte Baïsse ◽  
Marta Bellone ◽  
Milica Gikic ◽  
Tatiana Smirnova ◽  
...  
Keyword(s):  
Acute Leukemia ◽  
Vascular Endothelium ◽  
Lymphoblastic Leukemia ◽  
Critical Role ◽  
Leukemia Cell ◽  
Hematologic Malignancies ◽  
Selectin Ligands ◽  
Blast Cells ◽  
Acute Myeloid

Acute myeloid and lymphoblastic leukemia are poor prognosis hematologic malignancies, which disseminate from the bone marrow into the blood. Blast interactions with selectins expressed by vascular endothelium promote the development of drug resistance and leukostasis. While the role of selectins in initiating leukemia blast adhesion is established, our knowledge of the involved selectin ligands is incomplete. Using various primary acute leukemia cells and U937 monoblasts, we identified here functional selectin ligands expressed by myeloblasts and lymphoblasts by performing biochemical studies, expression inhibition by RNA interference and flow adhesion assays on recombinant selectins or selectin ligands immunoadsorbed from primary blast cells. Results demonstrate that P-selectin glycoprotein ligand-1 (PSGL-1) is the major P-selectin ligand on myeloblasts, while it is much less frequently expressed and used by lymphoblasts to interact with endothelial selectins. To roll on E-selectin, myeloblasts use PSGL-1, CD44, and CD43 to various extents and the contribution of these ligands varies strongly among patients. In contrast, the interactions of PSGL-1-deficient lymphoblasts with E-selectin are mainly supported by CD43 and/or CD44. By identifying key selectin ligands expressed by acute leukemia blasts, this study offers novel insight into their involvement in mediating acute leukemia cell adhesion with vascular endothelium and may identify novel therapeutic targets.

Role of the Flt-1 receptor tyrosine kinase in regulating the assembly of vascular endothelium

Nature ◽  
1995 ◽  
Vol 376 (6535) ◽  
pp. 66-70 ◽  
Author(s):  
Guo-Hua Fong ◽  
Janet Rossant ◽  
Marina Gertsenstein ◽  
Martin L. Breitman
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Vascular Endothelium

scholarly journals Serum from Varicose Patients Induces Senescence-Related Dysfunction of Vascular Endothelium Generating Local and Systemic Proinflammatory Conditions

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Justyna Mikuła-Pietrasik ◽  
Paweł Uruski ◽  
Krzysztof Aniukiewicz ◽  
Patrycja Sosińska ◽  
Zbigniew Krasiński ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelium ◽  
Varicose Veins ◽  
Neutralizing Antibody ◽  
Biological Properties ◽  
Oxygen Species ◽  
Healthy Donors ◽  
Pai 1

Although the role of endothelium in varicose vein development is indisputable, the effect of the pathology on biological properties of endothelial cells remains unclear. Here we examined if the presence of varicose veins affects senescence of endothelial cells (HUVECs) and, if so, what will be the local and systemic outcome of this effect. Experiments showed that HUVECs subjected to serum from varicose patients display improved proliferation, increased expression of senescence marker, SA-β-Gal, and increased generation of reactive oxygen species (ROS), as compared with serum from healthy donors. Both increased SA-β-Gal activity and ROS release were mediated by TGF-β1, the concentration of which in varicose serum was elevated and the activity of which in vitro was prevented using specific neutralizing antibody. Senescent HUVECs exposed to varicose serum generated increased amounts of ICAM-1, VCAM-1, P-selectin, uPA, PAI-1, and ET-1. Direct comparison of sera from varicose and healthy donors showed that pathological serum contained increased level of ICAM-1, VCAM-1, P-selectin, uPA, and ET-1. Calendar age of healthy subjects correlated positively with serum uPA and negatively with P-selectin. Age of varicose patients correlated positively with ICAM-1, VCAM-1, and ET-1. Collectively, our findings indicate that the presence of varicose veins causes a senescence-related dysfunction of vascular endothelium, which leads to the development of local and systemic proinflammatory environment.

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