The role of factor XIII in fibroblast proliferation

Ueyama, Mamoru; Amano, Hisao; Hirakawa, Shun; Urayama, Tsutomu

doi:10.2491/jjsth1970.10.505

Cited by 15 publications

(20 citation statements)

References 8 publications

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“…The aim of the study was the detection and exact localization of Factor XIII subunit a (FXIII A) during the sequence of the stages. FXIII A seems to be an important factor in homeostasis of connective tissues, not only as a stimulator of fibroblast proliferation (Ueyama & Urayama, 1977;Bruhn et al, 1981), but also as a significant regulator of collagen synthesis by fibroblasts (Paye et al, 1989(Paye et al, , 1990) and as a crosslinking enzyme in collagen/fibronectin interactions (Keski-Oja et al, 1976;Mosher, 1976Mosher, , 1984Mosher et a!., 1979). The fact that wound healing was abnormal in FXIII-deficient patients (Duckert, 1972) agrees well with these experimental findings.…”

Section: Introductionmentioning

confidence: 58%

Accumulation of cells containing factor XIII subunit a around the foci of intense fibrosis in human epulides

et al. 1995

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On the basis of clinical and biochemical findings, Factor XIII subunit a (FXIII A) has been conjectured to play an important role in fibrotic processes. Epulis samples at different stages of fibrotic tissue formation were used as a model system for studying the localization and tissue distribution of FXIII A during the course of connective tissue generation. Marker characteristics of cells containing FXIII A (FXIII A+ cells) were determined as well. In double immunofluorescent labelling systems, FXIII A was localized in monocyte-derived (CD-14+), activated (HLA-DR+), and phagocytosing (Ki-M7+) tissue macrophages, which are widely distributed homogeneously in granulation tissues, but start to accumulate around foci of fibrosis as soon as the foci appear. During the relatively long process of fibrosis, FXIII A+ macrophages continuously decrease in number, and their morphological appearance changes from stellate to spindle-shaped. The nuclei of these cells were not labelled by Ki-67 monoclonal antibody; this indicating that they represent a non-proliferating cell population in the connective tissue stroma. The present findings may help to link theories concerning the role of FXIII A and those of macrophages in the connective tissue formation so far found separately in the literature.

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Section: Introductionmentioning

confidence: 58%

Accumulation of cells containing factor XIII subunit a around the foci of intense fibrosis in human epulides

et al. 1995

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“…This fibrin matrix formation is considered to be essential for the tissue repair, followed by the migration and proliferation of fibroblasts into the matrix. From in vitro study results with fibroblasts, FXIII is suggested to promote the proliferation of fibroblasts by changing the structure of the fibrin network [11,12].…”

Section: Discussionmentioning

confidence: 99%

Involvement of blood coagulation factor XIII in burn healing in the carbon tetrachloride-induced hepatic injury model in rats

et al. 1995

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An involvement of blood coagulation factor XIII (FXIII) in healing of burns was examined in rats with the carbon tetrachloride (CCl4)-induced hepatic injury. The oral administration of 2 and 4 ml/kg CCl4 to rats every 4 days delayed healing of the burns induced on the back skin and decreased FXIII activity. These animals showed some hepatotoxic signs (increased glutamic-oxaloacetic and glutamic-pyruvic transaminases) and accelerated blood coagulation system (increased fibrino-peptide A and fibrin degradation product). The delay in the burn healing was shortened by repeated intravenous injections with normal human placenta-derived FXIII concentrate (Fibrogammin P; 120 U/body) every 4 days. There was a negative correlation between plasma FXIII activity at the end of experiment and the time required for wound healing. These findings suggest that reduction in FXIII activity may be one of the factors inducing delayed wound healing in the CCl4-induced hepatic injury rats.

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“…This effect was reversed by the addition of purified fibronectin before clotting, suggesting that the fibronectin needs to be covalently cross-linked to fibrin by transglutaminase. The importance of this enzyme has been demonstrated in vitro (4,14,33) where optimal growth on clots requires the presence of the enzyme. Individuals with an inherited deficiency of the enzyme display poor wound-healing (1,6).…”

Section: Discussionmentioning

confidence: 99%

Role of fibronectin in the migration of fibroblasts into plasma clots.

Knox¹,

Crooks²,

Rimmer³

1986

The Journal of Cell Biology

116

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Abstract. The adhesion and migration of human diploid fibroblasts on plasma clots were measured. The role of plasma fibronectin was examined by depleting plasma of fibronectin before clotting. Fibronectin was not essential for cell adhesion and spreading, although rates were slightly slower on depleted dots. Rates of migration on the surface of clots were unaffected by fibronectin depletion.In contrast, fibronectin was an absolute requirement for migration of cells into plasma clots. Cells migrated rapidly into control clots but completely failed to penetrate the surface of fibronectin-depleted clots. The effect of depletion could only be reversed by adding fibronectin to depleted plasma before clotting. Adsorption of fibronectin after dotting failed to reverse the effect of depletion, suggesting that fibronectin had to be cross-linked by transglutaminase during the clotting process.

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The role of factor XIII in fibroblast proliferation

Cited by 15 publications

References 8 publications

Accumulation of cells containing factor XIII subunit a around the foci of intense fibrosis in human epulides

Accumulation of cells containing factor XIII subunit a around the foci of intense fibrosis in human epulides

Involvement of blood coagulation factor XIII in burn healing in the carbon tetrachloride-induced hepatic injury model in rats

Role of fibronectin in the migration of fibroblasts into plasma clots.

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