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1

The molecular mechanisms of post-adhesive transmigration of T cells

100%
Masuyama J.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 2
121-128
EN
Leukocyte extravasation is an essential phenomenon in inflammatory responses of the body. However, less is known about the mechanisms of transendothelial migration of leukocytes subsequent to their adhesion to the endothelium. It could be considered that at least three different cellular responses participate in the transmigration of adherent leukocytes: 1) polarization of adherent cells in cell shape, 2) interactions between adherent cells and molecules bound to the endothelial surface to stimulate migration through the junction between adjacent endothelial cells, and 3) co-ordination with endothelial cells to open the junction. Molecules involved in these events are discussed in this review.
2

Contribution of endothelial cells to immune processes.Influence of viral infection

100%
Zaczynska E.
Postępy Higieny i Medycyny Doświadczalnej
|
1994
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vol. 48
|
issue 3
243-257
EN
Contribution of endothelial cells to normal immune processes (circulation of leukocytes, immune diapedesis, presentation of antigenes) as well as to pathology caused by viral diseases is described.Cytokine secretion and expression of adhesion molecules, particularly during viral infections are described.Permissiveness of endothelial cells to HIV infection is presented.Contrinution of herperviruses (CMV, HSV) to thrombosis and atherosclerosos is also considered.
3

The influence of hypoxia on blood vessels endothelial cell function in brain

100%
Josko J., Gwozdz B.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
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vol. 57
|
issue 4
445-454
EN
Regardless of reason, endothelial cells hypoxia is a primary source of their dysfunction. The result of hypoxia is a damage of endothelium structure, that leads to neurons damage. Parallel to the hypoxia, the protective mechanisms are activated in order to decrease effect of endothelium and neurons damage.
4

The role of oxidatively modified low density lipoprotein in the pathogenesis of atherosclerosis

88%
Siennicka A., Zapolska-Downar D.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
vol. 57
|
issue 2
219-237
EN
The precise mechanisms of LDL oxidation in vivo are not well-known but the presence of several enzymes and agents capable of modifying LDL particles was noted in arterial wall. These reactive agents modify lipid, protein as well as antioxidant component of the LDL particles. Postsecretory modification in LDL structure trigger its atherogenic potential. LDL particles retained in the artery wall interact with the various forms of proteoglycans in the extracellular matrix, that increases the resident time of LDL in endothelial space and allows extensive modification. The modified forms of LDL are able to activate intimal cells and to trigger various inflammatory signals. In turn, activated intimal cells can secrete enzymes and agents capable of modifying LDL. These processes can initiate and maintain a vicious circle in the intima and lead to lesion progression.
5

Biomechanic shear stress in carotid arteries and atherosclerosis development

88%
Kazmierski R.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
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vol. 57
|
issue 6
713-725
EN
One of the major hemodynamic forces acting on blood vessels is shear stress, which is, the friction force between the endothelial cell surface and flowing blood. Arterial shear stress within physiologic range (15-70 dyne/cm2) induces endothelial quiescence and an atheroprotective gene expression profile. Low shear stress (< 4 dyne/cm2 ) stimulates atherogenic phenotype, whereas, high shear stress (>70 dyne/cm2 ) induce prothrombotic state.
6

How endothelial cell organo-specificity mediates circulating cell homing

88%
Kieda C.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
|
issue 2
81-89
EN
Normal and transformed cells are homing from the circulation into tissues in a very selective way thanks to highly complex molecular mechanisms that govern cell-to-cell interactions and drive the homing of circulating cells to be achieved properly. Because this is characterised by a resulting high selectivity, it constitutes a template for targeted drug-, gene- or cell-therapy strategies. Designing a mimetic-based therapy requires the identification of the responsible selective molecules but also, their mechanisms of action and interactions with their ligands, together with their biological modulation and regulation. This homing/invasion event happens to be decisive at the level of the endothelium that lines the vessel walls. Since cell-to-cell interactions mean a double recognition process, this review will illustrate the part played by the endothelial cells (EC) and their adhesion molecules: the protein as well as the glycan part point of view, the chronology and environmental modulation of EC adhesion molecules expression. These characteristics should provide keys to understand the resulting overall specificity of cell localisation. Taking into account the cytokine microenvironment, it was recently documented a fundamental role for locally secreted chemokines which act through their restricted presentation by endothelial cells. As such, chemokines contribute to illustrate the concept of endothelial organo-specificity which is approached here uncovering the role of glycoconjugates signalling as the hallmark of refined cellular recognitions and discussed, in the context of potential drug design against site-directed diseases as metastases, inflammatory leukocytes recruitment, tumour/inflammation-induced angiogenesis.
7

P-selectin mediates adhesion of leukocytes, platelets, and cancer cells in inflammation, thrombosis, and cancer growth and metastasis

51%
Chen M., Geng J.-G.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
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vol. 54
|
issue 2
75-84
EN
Stimulated endothelial cells and activated platelets express P-selectin (CD62P), a member of the selectin family of cell adhesion molecules, which interacts with P-selectin glycoprotein ligand-1 (PSGL-1, CD162) for leukocyte rolling on stimulated endothelial cells and heterotypic aggregation of activated platelets onto leukocytes. Cross-linking of PSGL-1 by P-selectin also primes leukocytes intracellularly for cytokine and chemoattractant-induced 2-integrin activation for firm adhesion of leukocytes. Furthermore, P-selectin mediates heterotypic aggregation of activated platelets to cancer cells and adhesion of cancer cells to stimulated endothelial cells. Here we provide a comprehensive summary of the functional roles and the biological importance of P-selectin-mediated cell adhesive interactions in the pathogeneses of inflammation, thrombosis, and the growth and metastasis of cancers.
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