Endothelial cell P-selectin mediates a proinflammatory and prothrombogenic phenotype in cerebral venules of sickle cell transgenic mice.

@article{Wood2004EndothelialCP,
  title={Endothelial cell P-selectin mediates a proinflammatory and prothrombogenic phenotype in cerebral venules of sickle cell transgenic mice.},
  author={Katherine C. Wood and Robert P. Hebbel and Daniel Neil Granger},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2004},
  volume={286 5},
  pages={
          H1608-14
        }
}
  • K. Wood, R. Hebbel, D. Granger
  • Published 1 May 2004
  • Biology, Medicine
  • American journal of physiology. Heart and circulatory physiology
Whereas the adhesion of leukocytes and erythrocytes to vascular endothelium has been implicated in the vasooclusive events associated with sickle cell disease, the role of platelet-vessel wall interactions in this process remains undefined. The objectives of this study were to: 1) determine whether the adhesion of platelets and leukocytes in cerebral venules differs between sickle cell transgenic (betaS) mice and their wild-type (WT) counterparts (C57Bl/6) under both resting and posthypoxic… 
View on PubMed
ajpheart.physiology.org
56 Citations
Highly Influential Citations
1
Background Citations
21
Methods Citations
1

56 Citations

Citation Type

Citation Type

The contribution of endothelial cell P-selectin to the microvascular flow of mouse sickle erythrocytes in vivo.
TLDR
It is concluded that endothelial cell P- selectin contributes to the microcirculatory abnormalities in sickle cell disease and that blocking P-selectin may be useful for preventing painful vasoocclusion in sickre cell disease.
Platelet P-selectin is significantly involved in leukocyte-endothelial cell interaction in murine antigen-induced arthritis
TLDR
These are the first in vivo results showing that the P-selectin stored in platelets is at least partly responsible for the leukocyte-endothelial cell interaction and the resulting tissue damage in AiA.
Role of Blood Cell–Associated AT1 Receptors in the Microvascular Responses to Hypercholesterolemia
TLDR
These data indicate that the platelet-vessel wall adhesion elicited by hypercholesterolemia is mediated by AT1a-R engagement on the endothelial cell rather than the platelets, whereas leukocyte recruitment ismediated by blood cell-associated AT1 a-R.
Short title: Endothelial P-selectin slows mouse sickle cell flow in vivo
TLDR
It is concluded that endothelial cell P-selectin contributes to the microcirculatory abnormalities in sickle cell disease and that blocking P- selectin may be useful for preventing painful vasoocclusion in sickling cell disease.
Endothelial cell NADPH oxidase mediates the cerebral microvascular dysfunction in sickle cell transgenic mice
  • K. Wood, R. Hebbel, D. Granger
  • Biology, Medicine
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2005
TLDR
Findings suggest that superoxide derived from endothelial cell NADPH‐oxidase and catalytically active iron contribute to the proinflammatory and prothrombogenic responses associated with sickle cell disease.
Mechanisms of enhanced thrombus formation in cerebral microvessels of mice expressing hemoglobin-S.
TLDR
The results indicate that the cerebral microvasculature is rendered vulnerable to thrombus formation in β(s) mice via a neutrophil-dependent mechanism that is associated with an increased formation of and enhanced platelet sensitivity toThrombin.
The Fucosylation Inhibitor, 2-Fluorofucose, Inhibits Vaso-Occlusion, Leukocyte-Endothelium Interactions and NF-ĸB Activation in Transgenic Sickle Mice
TLDR
2-Fluorofucose may be beneficial for preventing or treating vaso-occlusive crises in SCD patients, and Pretreatment with 2FF completely eliminated heme-induced lethality in HbSS-Townes mice, consistent with the observed anti-inflammatory and anti-adhesive properties of 2FF inSCD mice.
Heme triggers TLR4 signaling leading to endothelial cell activation and vaso-occlusion in murine sickle cell disease.
TLDR
It is concluded that intravascular hemolysis in SCD releases heme that activates endothelial TLR4 signaling leading to WPB degranulation, NF-κB activation, and vaso-occlusion, and heme lethality.
Platelet–Vessel Wall Interactions in the Microcirculation
TLDR
The interactions between platelets and the walls of microscopic blood vessels appear to have important implications in the initiation and/or progression of tissue injury associated with different experimental models of human disease.
Levels of soluble endothelium‐derived adhesion molecules in patients with sickle cell disease are associated with pulmonary hypertension, organ dysfunction, and mortality
TLDR
It is found that higher levels of soluble vascular cell adhesion molecule‐1 (sVCAM‐1) were associated with markers indicating renal dysfunction and hepatic impairment, and increased soluble adhesion molecules expression correlated with severity of pulmonary hypertension, a clinical manifestation of endothelial dysfunction.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 58 REFERENCES
Hypercholesterolemia Promotes P-Selectin–Dependent Platelet–Endothelial Cell Adhesion in Postcapillary Venules
TLDR
It is indicated that elevated cholesterol levels promote P/E adhesion in postcapillary venules and that whereas both endothelial and platelet P-selectin contribute to hypercholesterolemia-induced recruitment of platelets, platelet-associated P- selectin seems to play a more important role in producing the prothrombogenic phenotype in venules.
Platelet-endothelial cell interactions during ischemia/reperfusion : The role of P-selectin
TLDR
First in vivo evidence is provided that platelets accumulate in the postischemic microvasculature early after reperfusion via P-selectin-ligand interactions, indicating that platelet recruitment and subsequent activation might play an important role in the pathogenesis of I/R injury.
Superoxide mediates endotoxin-induced platelet-endothelial cell adhesion in intestinal venules.
TLDR
Findings indicate that neutrophil-derived superoxide plays a major role in the modulation of endotoxin-induced P/E adhesion in murine intestinal venules.
Nitric oxide modulates endotoxin-induced platelet-endothelial cell adhesion in intestinal venules.
TLDR
Findings indicate that eNOS-derived NO attenuates endotoxin-induced P/E adhesion and 2) sGC is responsible for the antiadhesive action of NO.
Hepatic leukostasis and hypoxic stress in adhesion molecule-deficient mice after gut ischemia/reperfusion.
TLDR
Results from adhesion molecule-deficient mice provide additional support for the view that LECA is an important determinant of the liver dysfunction induced by gut I/R.
Thrombospondin mediates adherence of CD36+ sickle reticulocytes to endothelial cells.
TLDR
The results indicate that TSP may be the major promoter of RBC adhesivity in plasma, and they suggest that therapeutic benefit might derive from interference with sickle reticulocyte CD36, as achieved by antibodies and CSVTCG in these studies.
Platelet-erythrocyte adhesion in sickle cell disease.
  • T. Wun, T. Paglieroni, +4 authors F. Tablin
  • Medicine, Biology
    Journal of investigative medicine : the official publication of the American Federation for Clinical Research
  • 1999
TLDR
Thrombospondin on sRBC may mediate, at least in part, sR BC-platelet adhesion in sickle cell disease, and the study of heterotypic cell-cell interactions is important in understanding the pathogenesis of vaso-occlusion in Sickle Cell disease.
Immunoneutralization of glycoprotein Ibalpha attenuates endotoxin-induced interactions of platelets and leukocytes with rat venular endothelium in vivo.
TLDR
These results provide the first evidence for involvement of GP Ibalpha in endotoxin-induced microvascular rolling of platelets and leukocytes, and this system serves as a potentially useful tool to examine GP I Balpha-associated function of human platelets in vivo.
Thrombospondin from activated platelets promotes sickle erythrocyte adherence to human microvascular endothelium under physiologic flow: a potential role for platelet activation in sickle cell vaso-occlusion.
TLDR
Activated platelet release factors, including alpha-granule TSP, which promote receptor-mediated sickle erythrocyte adherence to microvascular endothelium are identified, which could contribute to vaso-occlusive complications by promoting ery throats adherence and microv vascular occlusion.
Circulating activated endothelial cells in sickle cell anemia.
TLDR
The studies suggest that the vascular endothelium is activated in patients with sickle cell anemia, regardless of clinical status, andhesion proteins on activated endothelial cells may have a role in the vascular pathology of Sickle cell disease.
...
1
2
3
4
5
...