Onset and distribution of factor XIII-containing cells in the mesenchyme of chorionic villi during early phase of human placentation

Kappelmayer, János; Bacskó, György; Kelemen, E; Adány, R

doi:10.1016/s0143-4004(05)80408-4

Cited by 16 publications

(11 citation statements)

References 28 publications

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“…The presence of macrophages (Hofbauer cells) in the human placenta has been recognized for a long time, 38,39 but their origin has been unknown. Our data revealed the presence of macrophages and macrophage committed progenitors in the chorionic plate of the placenta even before fetoplacental circulation has started, suggesting that the macrophages may be generated de novo in the placenta and later migrate to the villi to promote the terminal maturation and enucleation of primitive RBCs.…”

mentioning

confidence: 99%

The first trimester human placenta is a site for terminal maturation of primitive erythroid cells

Handel

Prashad

Hassanzadeh-Kiabi

et al. 2010

Blood

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IntroductionThe hematopoietic system during embryonic development provides two important functions: rapid generation of terminally differentiated blood cells for the survival and growth of the embryo and establishment of a pool of undifferentiated hematopoietic stem cells (HSCs) for postnatal life. To achieve these goals, embryonic hematopoiesis is segregated into multiple waves that occur in several anatomical sites, 1 a process that is broadly conserved in vertebrates. 2,3 The yolk sac is the site of the first wave of embryonic hematopoiesis that generates both primitive red blood cells (RBCs) that deliver oxygen to the embryo and macrophages that assist in tissue remodeling and immune defense. 4 The second wave of hematopoiesis also commences in the yolk sac with the production of a transient pool of erythromyeloid progenitors. Although they lack self-renewal ability and lymphoid potential, they have an important function in fetal hematopoiesis as they rapidly differentiate into mature definitive erythroid and myeloid cells after migration to the fetal liver. 5,6 The third wave of hematopoiesis emerges in the major intra-and extraembryonic arteries, generating HSCs that can both self-renew and differentiate into all blood cell types, including lymphoid cells. HSCs subsequently colonize the fetal liver where they expand before eventually seeding the bone marrow. HSCs emerge in the AGM (aorta-gonad-mesonephros region) and attached vitelline and umbilical arteries, 7-11 the yolk sac, and the placenta. The capacity of the placenta for generation 12 and expansion 13-15 of multipotential hematopoietic stem/progenitor cells has been described recently in both mouse and human, [16][17][18] whereas its potential function as a primitive hematopoietic organ has not been evaluated.The most important products of primitive hematopoiesis that are critical for the survival of the embryo are the primitive RBCs. Experimental evidence suggests that the yolk sac-derived primitive erythroid cells are specified directly from mesoderm with restricted hematopoietic potential, rather than from a multipotential HSC. [19][20][21][22] Primitive red cells differ from definitive red cells not only in their developmental origin, but also in their larger size and distinct globin expression pattern. 23 In mice, primitive RBCs can be identified by expression of ⑀y-globin, 24 which is absent from definitive red cells derived from the fetal liver and the adult bone marrow that express ␤-major globin. 25 In human, primitive red cells uniquely express the ␣-like -globin as well as the ␤-like ⑀-globin. 26 Furthermore, primitive red cells differ from definitive red cells in that they enter circulation as nucleated erythroblasts, whereas the definitive erythroid cells complete maturation and enucleation in their site of origin, the fetal liver 27 or bone marrow, before entering circulation (reviewed in Chasis 28 ). It has been documented that this process occurs in "erythroblast islands" in association with macrophages, which digest the ejected RBC ...

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mentioning

confidence: 99%

The first trimester human placenta is a site for terminal maturation of primitive erythroid cells

Handel

Prashad

Hassanzadeh-Kiabi

et al. 2010

Blood

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“…Similar to these events during the early phase of human placentation, cells containing factor XIII A characterized as macrophages (tissue histiocytes, Hofbauer cells) are homogeneously scattered in the immature mesenchymal connective tissue, but from the eighth week of gestation they tend to accumulate in the peripheral part of the chorionic villi, while the central mesenchyme, which they surround, shows intense fibrotic changes. 56 These findings may help link theories concerning the role of factor XIII A and those of macrophages in the connective tissue formation so far found separately in the literature.…”

Section: Monocytes/macrophagesmentioning

confidence: 64%

“…If) from the early monocytic precursors in the bone marrow 43 to fixed (connective tissue histiocytes, pericytes, tumor associated macrophages, dermal dendrocytes, dendritic reticulum cells of lymph nodes, osteoclasts) and mobile (amniotic fluid, synovial fluid, peritoneal, pericardial and alveolar fluid) monocytederived mature macrophages representing the end stage of the differentiation of this cell line, 45,[47][48][49][50][51][52][53][54][55] we demonstrated that factor XIII A is found in different organs (uterus, prostate, placenta, etc) also in intracellular local- ization, ie, in cells expressing marker antigens characteristic for tissue macrophages (histiocytes). 56 ' 57 The pattern of staining for factor XIII A in bone marrow was found to be uniform in monocytic cells simultaneously labelled for factor XIII A and Leu M3. Diffuse cyto-plasmic granular localization was consistently observed at various stages of differentiation and labeling became more intensive during the progression of maturation.…”

Section: Monocytes/macrophagesmentioning

confidence: 96%

Intracellular Factor XIII: Cellular Distribution of Factor XIII Subunit a in Humans

Ádány¹

1996

Semin Thromb Hemost

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“…Besides hemostasis, FXIII seems also to play important roles in phagocytosis12 and tissue repair 13. Furthermore, FXIII is important in maintaining pregnancies,14,15 as deficiencies are associated with a higher rate of miscarriages 16. FXIII deficiency has also been shown to be associated with poor wound healing17–19 and angiogenesis 20,21.…”

Section: Introductionmentioning

confidence: 99%

Catridecacog: a breakthrough in the treatment of congenital factor XIII A-subunit deficiency?

Korte¹

2014

JBM

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Circulating factor XIII (FXIII) consists of two active (A) and two carrier (B) subunits in tetrameric form. Congenital FXIII deficiency is a rare autosomal-recessive trait that mostly results from an FXIII A-subunit deficiency. Classic coagulation assays, such as prothrombin time or activated partial thromboplastin time, are not sensitive to FXIII; therefore, specific FXIII assays are necessary to detect the deficiency. The clinical picture of congenital FXIII deficiency comprises abortions, umbilical cord bleeding, increased surgical bleeding, intracerebral hemorrhage (which can, unfortunately, be the very first sign of severe FXIII deficiency), menorrhagia, and wound-healing disorders. Given the risk of intracranial hemorrhage, continued prophylaxis is to be recommended in severe deficiency, even in the actual absence of bleeding symptoms. Functional FXIII half-life decreases in consumptive processes (eg, surgery), explaining why increased dosing is needed in such situations. A recombinant FXIII (rFXIII) subunit-A molecule, which is expressed in Saccharomyces cerevisiae, has been evaluated for replacement therapy in congenital FXIII deficiency. The bleeding frequency under continued rFXIII prophylaxis during a year-long treatment period was significantly lower compared to on-demand treatment. Importantly, no severe spontaneous bleedings occurred, and bleeding requiring additional intervention only occurred after relevant trauma. Treatment with rFXIII proved to be safe: antibodies against rFXIII detected in four patients were not considered clinically relevant. No allergic reactions were observed. These data show that rFXIII can be used safely and effectively for continued prophylaxis in congenital FXIII deficiency; it is conceivable that this also holds true for treatment of acute bleeding, but clinical proof of this is pending.

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Onset and distribution of factor XIII-containing cells in the mesenchyme of chorionic villi during early phase of human placentation

Cited by 16 publications

References 28 publications

The first trimester human placenta is a site for terminal maturation of primitive erythroid cells

The first trimester human placenta is a site for terminal maturation of primitive erythroid cells

Intracellular Factor XIII: Cellular Distribution of Factor XIII Subunit a in Humans

Catridecacog: a breakthrough in the treatment of congenital factor XIII A-subunit deficiency?

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