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L Camoin-Jau

Publications and source records attributed to L Camoin-Jau.

6 recordsLinked to original sources
PubMed2002

Platelet associated u-PA up-regulates u-PA synthesis by endothelial cells.

Adhesion of platelets to endothelium has been shown to induce important changes in endothelial properties. In this study, we examined the effect of platelet-endothelial cell interactions on the expression of urokinase-type plasminogen activator (u-PA) by human microvascular endothelial cells. After incubation of endothelial cells with platelets, a dose-dependent increase in the expression of u-PA Ag was observed and reached a plateau for a ratio of 300 platelets per endothelial cells. The u-PA Ag upregulation resulted from an increase in u-PA mRNA that originated from a synthesis by endothelial cells since no u-PA mRNA was detected in platelets. The platelet-induced u-PA synthesis was inhibited when the endothelial cells were pre-treated with phospholipase C to remove the u-PA receptor, or when the platelets were incubated with an antibody that blocks the binding of u-PA to u-PAR. Taken together, these data indicate that u-PA present on the platelet surface interacts with u-PAR on the endothelial cells and induces the u-PA synthesis. This mechanism may represent a physiological control of platelet-mediated intravascular fibrin deposition.

Adenosine Diphosphate↗
PubMed1999

Differences in levels of soluble E-selectin and VCAM-1 in malignant versus non malignant Mediterranean spotted fever.

In the present study, we investigated the plasma levels of soluble adhesion molecules E-selectin, P-selectin, intercellular adhesion molecule- (ICAM- ) and vascular cell adhesion molecule-1(VCAM-1) in 24 patients with Mediterranean spotted fever (MSF), 6 of whom with a malignant form. Measurements were performed on blood samples collected before treatment (T1), then twice during treatment (T2 and T3). Before treatment, MSF patients taken as a whole presented elevated levels of sICAM-1 and sVCAM-1 and normal levels of sE-selectin and sP-selectin compared to healthy controls. We found that sICAM-1 was elevated both in mild and malignant MSF. sE-selectin and sVCAM-1 were elevated only in patients with the malignant form and allowed to discriminate the two clinical subgroups. Their levels decreased after treatment with sE-selectin reaching control values at T2 whereas sVCAM-1 remained higher over the course of the malignant form. In patients with mild MSF, sP-selectin steadily increased after treatment, whereas it did not present any modification at any of the two sampling times in patients with the malignant form. Raised plasma levels of sE-selectin and sVCAM-1 reflect endothelial activation in malignant rickettsial disease and may be sufficiently early markers to influence the therapeutic decision.

Adult↗
PubMed1998

Activation of human endothelial cells via S-endo-1 antigen (CD146) stimulates the tyrosine phosphorylation of focal adhesion kinase p125(FAK).

S-Endo-1 antigen (CD146), a transmembrane receptor also known as MUC18/MCAM, is a member of the immunoglobulin superfamily and belongs to a group of cell adhesion molecules. CD146 is highly expressed on the whole vascular tree. We demonstrate here that engagement of CD146 on human endothelial cells isolated from cord blood results in tyrosine phosphorylation of a large panel of cellular proteins, although no tyrosine phosphorylation of CD146 was detected. In particular, CD146 cross-linking induces the tyrosine phosphorylation of the protein tyrosine kinase p125(FAK) as well as p125(FAK) association with paxillin, both events being inhibited by cytochalasin D. No direct association of CD146 with p125(FAK) was observed. Consistent with these data, CD146 associates with p59(fyn), a Src family kinase known to phosphorylate p125(FAK). The identification of a signaling pathway initiated by CD146 engagement and which includes p59(fyn), p125(FAK), and paxillin indicates that CD146 participates in outside-in signaling in endothelial cells.

Antigens, CD↗