Anticoagulant properties of annexin A5 are a consequence of crystallization, which forms the lattice over phospholipid surface. Crystallization of annexin A5 has been proven on homogeneous synthetic phospholipids. In our study, the crystallization of annexin A5 on inhomogeneous, naturally derived phospholipid surfaces has been reported for the first time. Crystallization of annexin A5 on different solid supported phospholipid bilayers was observed by atomic force microscopy. Our results support the putative role of annexin A5 crystal structures as possible antithrombotic shield.
COBISS.SI-ID: 22804519
Enhanced microvesiculation of cell membranes, as detected by reduced membrane adhesion, can contribute to hypercoagulability. IgG against beta2-glycoprotiein I (anti-beta2GPI) significantly reduced beta2-GPI-induced membrane adhesion, suggesting a direct role of anti-beta2-GPI in enhancing membrane microvesiculation. Nadroparin completely restored beta2-GPI-induced membrane adhesion in the presence of IgG anti-beta2-GPI. A novel anticoagulant mechanism of nadroparin is suggested that supplements its direct effect on the coagulation cascade.
COBISS.SI-ID: 26095321
We presented an overview of beta2-glycoprotein I (beta2-GPI) and annexin A5 (AnxA5)-phospholipid interactions including candidate beta2-GPI receptors, and their relevance for physiological processes. Both beta2-GPI and AnxA5 have thrombomodulatory functions in vivo. Antibodies against beta2-GPI and AnxA5 are particularly important in antiphospholipid syndrome. Expanding knowledge on beta2-GPI and AnxA5-phospholipid interactions will be a basis of future alternative therapies of antiphospholipid syndrome.
COBISS.SI-ID: 26136025
The synthesis of acute-phase protein serum amyloid A (SAA) is largely regulated by inflammation-associated cytokines. However, SAA is also synthesized in human carcinoma metastases and cancer cell lines. In vitro data supports involvement of SAA in neoplastic diseases. SAA might be included in a group of biomarkers that reflect malignancy and host response. This review provides a broad overview of ways that SAA could contribute to tumor development, progression, and metastasis, and to gain a better understanding of SAA as a possible link between chronic inflammation and neoplasia.
COBISS.SI-ID: 24710105
Overview of histopathologic findings in antiphospholipid syndrome (APS) is presented. Based on autopsy and biopsy studies, we propose a novel categorization of histopathologic lesions that occur in patients with APS. In addition to the already accepted category of microvascular thrombotic lesions, microangiopathic lesions consistent with thrombotic microangiopathy are proposed to be included in new revised classification criteria for APS. These findings support two main mechanisms in the pathogenesis of APS: endothelial cell activation and activation of coagulation cascade.
COBISS.SI-ID: 25266137