On the Retraction of Collagen and Fibrin Induced by Normal, Defective and Modified Platelets

Jeleńska, M.M.; Kopeć, M; Breddin, K

doi:10.1159/000215140

Cited by 12 publications

(8 citation statements)

References 26 publications

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“…The role of platelet FXIII in clot retraction is not clear. Platelet clot retraction of FXIII-deficient patients was found to be normal (162,306) or even enhanced (274). In contrast, reduced contractile force was measured in plateletrich plasma clot from a FXIII-deficient patient (57), and the combination of FXIII-A-deficient plasma with normal platelets was sufficient to impair isometric contraction of platelet-rich plasma clot (66).…”

Section: A Involvement Of Factor XIII In Platelet Functionmentioning

confidence: 99%

Factor XIII: A Coagulation Factor With Multiple Plasmatic and Cellular Functions

Muszbek

Bereczky

Bagoly

et al. 2011

Physiological Reviews

405

437

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Factor XIII (FXIII) is unique among clotting factors for a number of reasons: 1) it is a protransglutaminase, which becomes activated in the last stage of coagulation; 2) it works on an insoluble substrate; 3) its potentially active subunit is also present in the cytoplasm of platelets, monocytes, monocyte-derived macrophages, dendritic cells, chondrocytes, osteoblasts, and osteocytes; and 4) in addition to its contribution to hemostasis, it has multiple extra- and intracellular functions. This review gives a general overview on the structure and activation of FXIII as well as on the biochemical function and downregulation of activated FXIII with emphasis on new developments in the last decade. New aspects of the traditional functions of FXIII, stabilization of fibrin clot, and protection of fibrin against fibrinolysis are summarized. The role of FXIII in maintaining pregnancy, its contribution to the wound healing process, and its proangiogenic function are reviewed in details. Special attention is given to new, less explored, but promising fields of FXIII research that include inhibition of vascular permeability, cardioprotection, and its role in cartilage and bone development. FXIII is also considered as an intracellular enzyme; a separate section is devoted to its intracellular activation, intracellular action, and involvement in platelet, monocyte/macrophage, and dendritic cell functions.

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Section: A Involvement Of Factor XIII In Platelet Functionmentioning

confidence: 99%

Factor XIII: A Coagulation Factor With Multiple Plasmatic and Cellular Functions

Muszbek

Bereczky

Bagoly

et al. 2011

Physiological Reviews

405

437

View full text Add to dashboard Cite

show abstract

“…Aside from altering the structure of the fibrin network, a possible role of fibronectin in blood clots is to mediate interactions between cells or platelets and fibrin. Thus, fibronectin as well as fibrin may interact with platelet α IIb β 3 during clot retraction, a function that is deficient in Glanzmann's thrombasthenia [41]. Fibrin cross‐linked to fibronectin by FXIIIa (fibronectin–fibrin) constitutes a three‐dimensional matrix that increases adhesion and spreading of fibroblasts compared with fibrin alone [42].…”

Section: Fibronectin and Blood Coagulationmentioning

confidence: 99%

Role of fibronectin assembly in platelet thrombus formation

Cho

Mosher

2006

Journal of Thrombosis and Haemostasis

111

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Summary. Fibronectin is a component of subendothelial matrices and abundant in plasma. A role of fibronectin in thrombogenesis has been suspected for three decades. Soluble fibronectin is assembled by adherent fibroblasts and platelets and thus converted to an insoluble form that mediates cell adhesion. Recently, in vivo studies using intravital videomicroscopy revealed that plasma fibronectin is important for stabilization of platelet aggregates after vascular injury. This review goes over roles of fibronectin in platelet functions with a focus on fibronectin assembly within developing platelet thrombi.

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“…5,6 In particular, platelets cause clot retraction (CR) by retracting extended filopodia along fibrin strands. 7 There have been conflicting reports about the effects of FXIII deficiency on CR; investigators reported that the absence of FXIII abolished, 7-9 did not affect, 10,11 or rather enhanced 12 CR in patients with congenital FXIII deficiency. However, platelet aggregation induced by various agents is uniformly normal in patients with congenital FXIII deficiency.…”

Section: Introductionmentioning

confidence: 99%

Impaired clot retraction in factor XIII A subunit–deficient mice

Kasahara

Souri

Kaneda

et al. 2010

Blood

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Factor XIII (FXIII) is a plasma transglutaminase that cross-links fibrin monomers, ␣ 2 -plasmin inhibitor, and so forth. Congenital FXIII deficiency causes lifelong bleeding symptoms. To understand the molecular pathology of FXIII deficiency in vivo, its knockout mice have been functionally analyzed. Because prolonged bleeding times, a sign of defective/abnormal primary hemostasis, were commonly observed in 2 separate lines of FXIII A subunit (FXIII-A) knockout mice, a possible role or roles of FXIII in platelet-related function was investigated in the present study. Although platelet aggregation induced by adenosine diphosphate or collagen was normal, clot retraction (CR) was lost in the platelet-rich plasma (PRP) of FXIII-A knockout mice. IntroductionCoagulation factor XIII (FXIII) is a pro-enzyme of plasma transglutaminase (TGase) consisting of 2 enzymatic A subunits (FXIII-A) and 2 noncatalytic B subunits, and plays a critical role in the generation of a stable hemostatic plug. 1-3 FXIII catalyzes intermolecular cross-linking reactions between fibrin monomers, ␣ 2 -plasmin inhibitor, fibronectin, etc. These reactions increase the mechanical strength of the fibrin clot and its resistance to proteolytic degradation, and enhance the assembly of the extracellular matrix.Congenital FXIII deficiency is a rare autosomal recessive disorder, the cases of most of which are caused by defects in the FXIII-A gene. 3 A lifelong bleeding tendency, abnormal wound healing, and recurrent spontaneous miscarriage are common symptoms of FXIII deficiency. 1,4 FXIII-A exists extracellularly in plasma as well as intracellularly as a cytosolic protein in megakaryocytes/platelets and monocytes/macrophages, although the function(s) of intracellular FXIII-A remain(s) unknown. 5,6 In particular, platelets cause clot retraction (CR) by retracting extended filopodia along fibrin strands. 7 There have been conflicting reports about the effects of FXIII deficiency on CR; investigators reported that the absence of FXIII abolished, 7-9 did not affect, 10,11 or rather enhanced 12 CR in patients with congenital FXIII deficiency. However, platelet aggregation induced by various agents is uniformly normal in patients with congenital FXIII deficiency. 8,9,13,14 To understand the precise molecular pathology of FXIII deficiency in vivo, FXIII-A knockout (KO) mice have been analyzed. FXIII-A KO mice demonstrated a severe bleeding tendency. 15 We also reported that FXIII-A KO mice developed severe uterine bleeding, resulting in spontaneous miscarriage in females, and male-specific intrathoracic hemorrhage as well as excessive cardiac fibrosis. 16,17 Because bleeding times in FXIII-A KO mice were longer than in wild-type, 15,18 we hypothesized that FXIII-A KO mice might have a defective platelet-related function(s). Accordingly, we have explored the contribution of FXIII to the process of CR in the present study. Methods AnimalWild-type C57BL/6J mice were obtained from Japan SLC Inc. Genetargeted mice of FXIII-A were generated as previously reported, ...

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On the Retraction of Collagen and Fibrin Induced by Normal, Defective and Modified Platelets

Cited by 12 publications

References 26 publications

Factor XIII: A Coagulation Factor With Multiple Plasmatic and Cellular Functions

Factor XIII: A Coagulation Factor With Multiple Plasmatic and Cellular Functions

Role of fibronectin assembly in platelet thrombus formation

Impaired clot retraction in factor XIII A subunit–deficient mice

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