Factor XIII and inflammatory cells

Bagoly, Zsuzsa; Katona, Éva; Muszbek, László

doi:10.1016/j.thromres.2012.02.040

Cited by 46 publications

(59 citation statements)

References 41 publications

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“…This relationship includes the modification of FXIII expression during monocyte differentiation and monocyte-macrophage activation, and is supported by the presence of FXIII in the cytoplasm of monocytes/macrophages with phagocytic potential. Cytoplasmic FXIII (cFXIII) is implicated in phagocytosis, and the effect of monocyte activation on cFXIII expression depends on the activation pathway: the classical pathway down-regulates cFXIII expression, while the alternative pathway up-regulates it (Bagoly, Katona &Muszbek, 2012). cFXIII produced by macrophages from the penumbra and core is a substrate for neutrophil elastase released by activated PMNs, inducing a limited cleavage of cFXIII, which results in enzyme activation, followed by a much slower proteolytic inactivation (Bagoly et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Inflammatory cell populations in early neuroinflammation in the core and peri-ischemic lesions of rat brain after transient focal cerebral ischemia: A morphometric study

Horváth

Orădan

Chiriac

et al. 2018

Preprint

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Background and Objective:Clinical and experimental observations emphasize the role of inflammation as a direct risk factor for stroke. To better characterize the inflammation, we have conducted a detailed histological analysis of the inflammatory cell population after transient middle cerebral artery occlusion in a rat model. Methods:Fifteen adult Wistar male rats were divided randomly into test (n=10) and sham (n=5) groups. In the ischemic group, transient focal cerebral ischemia was induced with an intraluminal filament technique. Histologic lesions of the ischemic core and the surrounding penumbra zone were evaluated, based on a complex algorithm. Representative morphological changes in the core and the penumbra zone were compared. Immunohistochemistry was performed for leukocytes markers (CD15, CD68, CD3), leukocyte-released effectors (MMP-9 and COX-2), and FXIII (possibly involved in microglia and macrophage activation)Results: Neuronal vacuolation and degeneration were significantly more in the core lesion, whereas cellular edema and inflammatory infiltrate were increased in the penumbra. CD68, CD3, FXIII and Cox-2 expression were significantly higher in the penumbra than in the core (p=0.026; p=0.006; p=0.002; and p<0.001).Discussion: In the rat model of middle cerebral artery occlusion, inflammatory mechanisms, microglia/macrophage cells, and T-lymphocytes likely play an important role in the penumbra. The deterioration of neurons is less in the penumbra than in the core. Appreciation of the role of the inflammatory cells and mechanisms involved in stroke might lead to measures to inhibit the injury and save brain volume. ABSTRACT Background and Objective: Clinical and experimental observations emphasize the role of inflammation as a direct risk factor for stroke. To better characterize the inflammation, we have conducted a detailed histological analysis of the inflammatory cell population after transient middle cerebral artery occlusion in a rat model.

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Section: Discussionmentioning

confidence: 99%

Inflammatory cell populations in early neuroinflammation in the core and peri-ischemic lesions of rat brain after transient focal cerebral ischemia: A morphometric study

Horváth

Orădan

Chiriac

et al. 2018

Preprint

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“…FXIII-A, as a potential active subunit is also present in the cytoplasm of platelets, monocytes, macrophages, dendritic cells, chondrocytes, osteoblasts, and osteocytes. It can be detected from the early stage of monoblasts in the bone marrow via blood monocytes to the connective tissue macrophages [4][5][6][7][8][9][10][11]. FXIII-A is considered as a positive marker protein of the cell line in which it acts as an intracellular transglutaminase with roles in various intracytoplasmatic and intranuclear processes.…”

Section: +mentioning

confidence: 99%

“…The role of intracellular FXIII-A in platelets, monocytes, macrophages, and other inflammatory cells is an open and widely discussed question. It was suggested that this factor is involved in intracellular presentation, distribution, and other possible activation of cells' secretion [2,6].…”

Section: +mentioning

confidence: 99%

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The role of factor XIII-A in the development of inflammatory skin lesions

2014

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Factor XIII (FXIII) is a unique clotting factor activated in the last stage of the coagulation cascade, with multiple other plasmatic and cellular functions, outside of the traditional homeostasis. Literature data show that FXIII is expressed in skin lesions in the course of various inflammatory skin disorders. Dermis contains a series of macrophages and dendritic cells, which express different phenotypes including FXIII. Increased levels of FXIII-positive cells are present in specific cutaneous inflammatory and fibrotic conditions. The aim of this review is to provide the relationship between FXIII and the development of the inflammatory skin lesions.

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“…Fibrin monomers polymerize through non-covalent interactions and by isopeptide bond formation between the monomers. This clot formation/stabilization is a common phenomenon also in inflammation [ [11], [12]]. The major route for elimination of fibrin clots is their proteolytic degradation by plasmin formed from plasma plasminogen by tissue plasminogen activator (tPA) [13] and this route is very sensitive to a variety of biomechanical, chemical and cellular factors [14].…”

Section: Introductionmentioning

confidence: 99%