Protein Z is not synthesised by human umbilical vein endothelial cells

Cesari, Francesca; Sofi, Francesco; Evangelisti, L; Gensini, Gian Franco; Abbate, Rosanna; Fedi, Sandra

doi:10.1016/j.thromres.2005.10.005

Cited by 2 publications

(2 citation statements)

References 9 publications

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“…Although this has not been confirmed by others [30], it could have been a confounder variable. Therefore, we looked for a possible correlation between PZ and VWF:Ag as a marker of endothelial damage.…”

Section: Discussioncontrasting

confidence: 68%

Plasma Protein Z and Protein C Inhibitors and Their Role in Hypercoagulability of Thalassemia

et al. 2007

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A hypercoagulable state has been described in thalassemia patients, partly due to a deficiency of inhibitors, protein C (PC) in particular. Since a potential role of a new hemostatic factor named protein Z (PZ) has been reported in hypercoagulability, we evaluated plasma PZ and PC levels in thalassemia and their possible relation to the hypercoagulable state. Sixty subjects with thalassemia major and 10 with thalassemia intermedia (TI) followed at our Department were enrolled in the study. An age-matched control group of healthy subjects was considered. PZ, thrombin-antithrombin complexes, PC concentration (PC:Ag) and activity (PC:Act) were measured. PZ, PC:Ag and PC:Act were significantly lower in thalassemia major and thalassemia intermedia subjects than in 30 healthy controls (p < 0.001), while thrombin-antithrombin complex levels were significantly increased (p < 0.001) and related to PC levels but not to PZ levels (p < 0.05). PZ and PC levels are reduced in thalassemia but only PC has an effect on the thalassemia hypercoagulable state.

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Section: Discussioncontrasting

confidence: 68%

Plasma Protein Z and Protein C Inhibitors and Their Role in Hypercoagulability of Thalassemia

et al. 2007

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“…Liver is the main source of this protein, as supported by the strong correlations between PZ and other plasma proteins of liver origin, and the severe deficiency of plasma PZ found in patients with liver disease (Kemkes‐Matthes & Matthes, 1995a). There are conflicting results on the expression of PZ by human endothelial cells (Cesari et al , 2006a; Vasse et al , 2006). The protein is synthesised with a prepro‐leader sequence, and the human mature protein contains 360 residues, has a molecular weight of 62 kDa, and a half‐life of approximately 2·5 d (Miletich & Broze, 1987).…”

Section: Protein Zmentioning

confidence: 99%

Protein Z/Z‐dependent protease inhibitor (PZ/ZPI) anticoagulant system and thrombosis

et al. 2007

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SummaryA new anticoagulant system involving a serpin has been recently characterised. The protein Z/Z-dependent protease inhibitor (PZ/ZPI) system inhibits activated factors X, XI and IX by different mechanisms. By homology with other anticoagulant systems (antithrombin or the protein C/protein S), deficiency of the serpin (ZPI) or its cofactor (PZ) might imbalance the haemostatic system with thrombotic consequences. Evidence supports the in vivo anticoagulant role of this complex and the thrombotic consequences of its deficiency. Non-sense variations of the ZPI (W303X and R67X) have been associated with increased risk of venous thrombosis. Moreover, PZ deficient mice carrying the FV Leiden have a thrombotic phenotype. Finally, some reports suggest that PZ deficiency might increase the risk of thrombosis. However, other studies question the thrombotic relevance of both ZPI and PZ deficiencies. This system could play a redundant role in haemostasis that explains the conflicting results on its thrombotic potential, which might be exacerbated in combination with other prothrombotic factors.

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Protein Z is not synthesised by human umbilical vein endothelial cells

Cited by 2 publications

References 9 publications

Plasma Protein Z and Protein C Inhibitors and Their Role in Hypercoagulability of Thalassemia

Plasma Protein Z and Protein C Inhibitors and Their Role in Hypercoagulability of Thalassemia

Protein Z/Z‐dependent protease inhibitor (PZ/ZPI) anticoagulant system and thrombosis

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