Browsing by Author "Campos, Manuel"
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- Circulating endothelial cells in patients with venous thromboembolism and myeloproliferative neoplasmsPublication . Torres, Cláudia; Fonseca, Ana Mafalda; Leander, Magdalena; Matos, Rui; Morais, Sara; Campos, Manuel; Lima, MargaridaBackground: Circulating endothelial cells (CEC) may be a biomarker of vascular injury and pro-thrombotic tendency, while circulating endothelial progenitor cells (CEP) may be an indicator for angiogenesis and vascular remodelling. However, there is not a universally accepted standardized protocol to identify and quantify these cells and its clinical relevancy remains to be established. Objectives: To quantify CEC and CEP in patients with venous thromboembolism (VTE) and with myeloproliferative neoplasms (MPN), to characterize the CEC for the expression of activation (CD54, CD62E) and procoagulant (CD142) markers and to investigate whether they correlate with other clinical and laboratory data. Patients and Methods: Sixteen patients with VTE, 17 patients with MPN and 20 healthy individuals were studied. The CEC and CEP were quantified and characterized in the blood using flow cytometry, and the demographic, clinical and laboratory data were obtained from hospital records. Results: We found the CEC counts were higher in both patient groups as compared to controls, whereas increased numbers of CEP were found only in patients with MPN. In addition, all disease groups had higher numbers of CD62E+ CEC as compared to controls, whereas only patients with VTE had increased numbers of CD142+ and CD54+ CEC. Moreover, the numbers of total and CD62+ CEC correlated positively with the white blood cells (WBC) counts in both groups of patients, while the numbers of CEP correlated positively with the WBC counts only in patients with MPN. In addition, in patients with VTE a positive correlation was found between the numbers of CD54+ CEC and the antithrombin levels, as well as between the CD142+ CEC counts and the number of thrombotic events. Conclusions: Our study suggests that CEC counts may reveal endothelial injury in patients with VTE and MPN and that CEC may express different activation-related phenotypes depending on the disease status.
- Role of the endothelial system in Bay-K-8644 enantiomer and nifedipine vasomodulator action in rat aortaPublication . Verde, Ignacio; Gil-Longo, José; Orallo, Francisco; Campos, Manuel; Calleja, José MariaThe potential importance of the endothelial system in regulating the effects of (−)-Bay K 8644 (0.1 μM), (+)-Bay K 8644 (0.1 μM) and nifedipine (10 nM) on resting tension, on contractile responses to noradrcnaline (NA) and Ca2+ (in a Ca2+-free high-K+ solution), and on basal, NA-induced and K+-induced 45Ca2+ uptake, was investigated in rat aorta rings. Mechanical removal of endothclium considerably potentiated the contractile response induced by NA in standard medium and by Ca2+ in Ca2+-free high-K' (15 mM) medium, but did not modify the response induced by Ca2+ in Ca2+-frcc high-K+ (55 mM) medium or by NA in Ca2+-free medium. Furthermore, the basal 45Ca2+ uptake and that induced by NA (10 μM) or KCl (15 and 55 mM) were similar in endothelium-rubbed and intact rings. (−)-Bay K 8644 (0.1 μM) shifted the NA and Ca2+ concentration-response curves to the left with potentialion of the maximal contraction. However, (+)-Bay K 8644 (0.1 μM) and nifedipine (10 nM) caused a shift to the right, with depression of the maximal contraction. The NA concentration-response curves, and those of Ca2+ in Ca2+-free high-K+ (55 mM) medium, were affected by the drugs to similar extents, and were not modified by the presence or absence of endothelial cells. The drugs tested did not affect resting tension. Basal 45Ca2+ uptake was not modified by either nifedipine or the Bay K 8644 enantiomers. On the other hand, (−)-Bay K 8644 increased with equal effectives both NA- and KCl-induccd 45Ca2+ uptake, whilst (+)-Qay K 8644 and nifedipine inhibited both uptakes. The presence or absence of endothelium did not modify these effects. These results suggest that, in rat aorta, the endothelial system does not modulate either the agonist effect of (−)-Bay K 8644 or the antagonistic effects of (+)-Bay K S644 and nifedipine. Furthermore, our data indicate that the effects of Bay K 8644 enantiomers and nifedipine on the contractile responses and 45Ca2+ uptake elicited by NA and high-K+ (55 mM) solutions are similar.