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T Kaji

Publications and source records attributed to T Kaji.

At least 91 records · Page 5Linked to original sources
PubMed1994

Plasmin-induced reduction of heparan sulfate in cultured vascular endothelial cell layer.

Plasmin-induced alteration of glycosaminoglycans (GAGs) was investigated using a cell culture system of vascular endothelial cells derived from bovine aorta. In the cell layer, the incorporation of [3H]glucosamine into GAGs, a marker of the sugar chain formation, was slightly decreased by plasmin. On the other hand, the incorporation of [35S]sulfate, a marker of the sulfation, was markedly decreased by the protease. Plasminogen also induced a weak but similar change. Characterization of the cellular GAGs showed that plasmin inhibited the incorporation of both [3H]glucosamine and [35S]sulfate into the major component heparan sulfate at a similar degree. In the other GAGs, the [35S]sulfate incorporation was significantly decreased by plasmin without a change of the [3H]glucosamine incorporation. The leakage of lactate dehydrogenase from the endothelial cells was significantly increased by plasmin, suggesting that the protease exhibited cytotoxicity. The present data suggest that the anticoagulant activity on the surface of vascular endothelium mediated by the anticoagulant heparan sulfate may be reduced by plasmin which will be generated from plasminogen by plasminogen activators derived from endothelial cells.

Animals↗
PubMed1994

Calcium regulation of tissue plasminogen activator and plasminogen activator inhibitor-1 release from cultured human vascular endothelial cells.

Tissue plasminogen activator (t-PA) produced by vascular endothelial cells converts plasminogen to plasmin which degrades fibrin. Since t-PA activity is greatly potentiated in the presence of fibrin (1,2), the activator is implicated in intravascular fibrinolysis. On the other hand, endothelial cells also produce plasminogen activator inhibitor-1 (PAI-1) (3). The inhibitor associated with vascular endothelium rapidly inhibits t-PA, while that released into the liquid phase has a little anti-activator activity (4). However, clinical studies have shown that elevation of plasma PAI-1 level is a risk factor of thrombosis (5,6). It is thus suggested that the balance between t-PA and PAI-1 is important for the regulation of fibrinolysis. The release of t-PA and PAI-1 from vascular endothelial cells is regulated by physiological factors including thrombin (3,7), histamine (8), vasoconstrictor peptide endothelins (9,10) and cytokines (11). In addition, the regulation of the t-PA release and that of the PAI-1 release are not necessarily coupled. It has been shown that activated protein kinase C and cyclic AMP are involved in the stimulation and suppression, respectively, of the endothelial t-PA and PAI-1 production (12,13). However, the role of intracellular calcium in the regulation of endothelial t-PA and PAI-1 release has remained to be elucidated. In the present study, we investigated the effect of calcium ionophore A23187 on the release of t-PA antigen (t-PA:Ag) and PAI-1 antigen (PAI-1:Ag) from cultured vascular endothelial cells derived from human umbilical vein.

Antigens↗
PubMed1994

Transforming growth factor beta-induced tolerance to cadmium cytotoxicity in cultured vascular endothelial cells.

We investigated whether or not transforming growth factor beta (TGF beta 1) affects the sensitivity to cadmium of bovine aortic endothelial cell in a culture system. Cadmium cytotoxicity was evaluated by [3H]adenine release assay. It was found that pretreatment with recombinant human TGF beta 1 (rhTGF beta 1) of the confluent cultures resulted in a reduction of cadmium cytotoxicity, suggesting that the cytokine induced a tolerance to cadmium in the cells. Such a tolerance was induced slightly by either recombinant human tumor necrosis factor alpha or recombinant human basic fibroblast growth factor but not by recombinant human interleukin-1 beta and -6; rhTGF beta 1 was the most potent inducer. rhTGF beta 1 failed to induce the tolerance in the presence of anti-rhTGF beta 1 antibody. Pretreatment with the antibody alone caused a significantly sensitive response to cadmium, suggesting that endogenous TGF beta 1 can physiologically contribute to protection against cadmium cytotoxicity in endothelial cells. The accumulation of cadmium was increased in the extracellular fraction but significantly decreased in the intracellular fraction of the cells by pretreatment with rhTGF beta 1. The cadmium content was significantly decreased in the particulate fraction but not in the cytosol fraction. Gel filtration chromatography of the cytosol fraction revealed that cadmium was bound to high-molecular-weight protein and metallothionein; both peaks were slightly increased by pretreatment with rhTGF beta 1. It was concluded that rhTGF beta 1 induces a tolerance to cadmium in cultured endothelial cells, caused by a decrease in the cadmium accumulation in the particulate fraction of the cells. TGF beta 1 may serve as a protective factor against cadmium cytotoxicity in vascular endothelial cells.

Animals↗
PubMed1994

Basic fibroblast growth factor suppresses tissue plasminogen activator release from cultured human umbilical vein endothelial cells but enhances that from cultured human aortic endothelial cells.

Since basic fibroblast growth factor (bFGF) modulates the functions of vascular endothelial cells, we hypothesized that this factor may be involved in the regulation of the blood coagulation-fibrinolytic system mediated by the cells. Confluent cultures of vascular endothelial cells from human umbilical vein were treated with recombinant human bFGF (bFGF) in a serum-free medium and the content of tissue plasminogen activator antigen (t-PA:Ag) in the medium was determined by EIA. Treatment with bFGF resulted in a significant decrease in the release of t-PA:Ag from the cells accompanied with a less t-PA activity in the medium. In contrast, the t-PA:Ag release from human aortic endothelial cells was significantly increased by bFGF. The bFGF-induced decrease in the t-PA:Ag release from the venous endothelial cells was completely blocked by anti-bFGF antibody. The incorporation of [3H]leucine into the acid-insoluble fraction of the cells was significantly increased by bFGF; however, the activity of lactate dehydrogenase leaked into the medium was significantly decreased, suggesting that the suppression of the t-PA:Ag release caused by bFGF in the venous endothelial cells was not due to either a nonspecific inhibition of protein synthesis or a nonspecific cell damage. Since bFGF is postulated to be released from damaged endothelial cells, the present data suggest the regulation by bFGF of hemostasis mediated by endothelial cells when the vascular endothelium was damaged.

Aorta↗
PubMed1994

Alteration of glycosaminoglycans induced by cadmium in cultured vascular smooth muscle cells.

Alteration of glycosaminoglycans (GAGs) in cultured bovine aortic smooth muscle cells after exposure to cadmium was investigated. It was revealed that cadmium increased the accumulation of GAGs metabolically labeled with [3H]glucosamine but decreased that with [35S]sulfate in the cell fraction, the cell surface fraction and the medium fraction. This suggested that cadmium stimulated the biosynthesis of GAGs but inhibited their sulfation in the cells. A similar alteration was observed in cadmium-treated human aortic smooth muscle cell layer. Of tested cations including cadmium, bismuth, cobalt, copper, lead, manganese, nickel and zinc, only cadmium stimulated [3H]glucosamine incorporation, with a strong inhibition of the [35S]sulfate incorporation in the bovine cells. Characterization of bovine smooth muscle GAGs showed that the cadmium-induced increase in the [3H]glucosamine incorporation was mainly observed in heparan sulfate; the inhibition of the [35S]sulfate incorporation occurred non-selectively. Cadmium accumulated in bovine vascular smooth muscle cells in a dose-dependent manner with an increase in the leakage of lactate dehydrogenase into the medium. The present data suggest that vascular smooth muscle cells respond to the cytotoxicity of cadmium and promote the GAG synthesis with a reduction of their sulfation. It is postulated that this response may be a defensive one to the damage of the vascular tissue caused by cadmium but would be a component of the metal-induced atherosclerosis.

Animals↗
PubMed1994

Suppression of plasminogen activator inhibitor type 1 release from cultured human umbilical vein endothelial cells by basic fibroblast growth factor.

We investigated the release of plasminogen activator inhibitor type 1 (PAI-1) from cultured vascular endothelial cells after exposure to basic fibroblast growth factor (bFGF). Treatment with human recombinant bFGF of confluent cultures of endothelial cells derived from human umbilical vein resulted in a reduction of the accumulation of PAI-1 antigen (PAI-1:Ag) in the conditioned medium. The suppressive effect of bFGF completely disappeared in the presence of anti-bFGF antibody. The reduction of endothelial PAI-1:Ag release induced by bFGF was suggested to be independent of intracellular accumulation of cyclic AMP. On the other hand, nordihydroguaiaretic acid (NDGA), an inhibitor of the lipoxygenase pathway of arachidonic acid metabolism, suppressed the spontaneous release of PAI-1:Ag by itself; in the presence of NDGA, bFGF failed to further suppress the PAI-1:Ag release. The effect of bFGF and indomethacin, an inhibitor of the cyclooxygenase pathway, was additive on the PAI-1:Ag release. The present data suggest that bFGF reduces the endothelial PAI-1:Ag release via suppression of the putative lipoxygenase pathway which up-regulates a part of the spontaneous PAI-1:Ag release.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1994

Stimulation by zinc of cultured vascular endothelial cell proliferation: possible involvement of endogenous basic fibroblast growth factor.

Vascular endothelial cells from bovine aorta were cultured with zinc sulfate (20 microM or less) for 24 h and labeled with [3H]thymidine or [14C]leucine during the last 3 h of the culture. It was found that the cell number was significantly increased by zinc alone; the incorporation of both [3H]thymidine and [14C]leucine was also stimulated by the metal. The stimulation by zinc occurred in the presence or absence of exogenous basic fibroblast growth factor (bFGF). However, other heavy metals including copper, manganese and nickel did not exhibit such a stimulatory effect, suggesting that zinc plays a particular role in endothelial cell proliferation. Stimulation of the [3H]thymidine incorporation by zinc disappeared in the presence of either cycloheximide or anti-bFGF IgG; in addition, a lipoxygenase inhibitor nordihydroguaiaretic acid diminished the zinc stimulation but a cyclooxygenase inhibitor indomethacin did not exhibit such an inhibitory effect. These results indicated that zinc stimulated the proliferation of endothelial cells through the lipoxygenase pathway which mediates the stimulation by endogenous bFGF. In other words, the metal may amplify the endogenous bFGF-dependent proliferation of the cells.

Animals↗
PubMed1994

Histological features of palatine tonsils in pustulosis palmaris et plantaris: a morphometric study.

The morphological expression of the immune response of palatine tonsils obtained from patients with pustulosis palmaris et plantaris (PPP) was investigated by morphometry in conjunction with immunohistochemistry. First, to differentiate the histological features of tonsils between PPP and habitual tonsillitis, each extent of the T cell dependent areas (T nodules), B cell dependent areas (lymph follicles), germinal centers, mixed areas of T cells and B cells, and lacunar epithelium was measured and compared on 38 patients with PPP and 47 with habitual tonsillitis, respectively. The most remarkable findings in PPP were enlargement of the secondary T nodules, and atrophy of the lymph follicles with a decrease in number of the germinal center cells and fibrosis. These changes of lymph follicles were similar to those in the older patients with habitual tonsillitis, which suggests the intensely advanced stage of the immune response within the tonsils. Second, the histological structures of the tonsils of 15 tonsillectomy effective cases (88.2%) was compared with those of two non-effective cases in curing skin lesions. The histological structure in the non-effective cases was very similar to that in habitual tonsillitis cases. This indicates that the histological findings may be useful in predicting the effects of tonsillectomy on PPP.

Adult↗
PubMed1994

Cadmium stimulation of glycosaminoglycan synthesis by cultured vascular endothelial cells: comparison of various cell types.

We investigated the effect of cadmium on the synthesis of glycosaminoglycans (GAGs) in confluent cultures of vascular endothelial cells derived from bovine aorta. Cadmium markedly increased the incorporation of [3H]glucosamine into GAGs in both the cell layer and the conditioned medium but decreased [35S]sulfate in the cell layer. This suggested that cadmium induced the GAG synthesis by endothelial cells accompanied by a reduction of the sulfation of cell-associated GAGs. Of the tested heavy metals, the [35S]sulfate incorporation in the cell layer was significantly decreased by lead; zinc slightly but significantly increased the [35S]sulfate incorporation; manganese and copper failed to change the [3H]glucosamine and [35S]sulfate incorporation; and the incorporation of [3H]glucosamine was increased only by cadmium. On the other hand, vascular smooth-muscle cells and fibroblastic Balb/3T3 cells responded to cadmium in a way similar to vascular endothelial cells, while fibroblastic IMR-90 cells, Chang liver cells and epithelial LLC-PK1 cells altered the [3H]glucosamine and [35S]sulfate incorporation after exposure to cadmium in different manners. The alteration of GAGs induced by cadmium may be involved in the pathogenesis of the metal.

Animals↗
PubMed1994

Dermatophilosis (Cutaneous streptothricosis) in Kafue lechwe (Kobus leche kafuensis).

Extensive dermatitis caused by Dermatophilus congolensis was identified in two kafue lechwe (Kobus leche kafuensis) in Lochinvar National Park of Zambia. The lesions were characterized by thickening of the skin, crusts, and nodfule formation. Almost all parts of the body were affected. Histologically there was an exudative dermatitis with acanthosis, parakeratosis, hyperkeratosis, and an exudate rich in neutrophils. This is the first known report of dermatophilosis in lechwe.

Actinomycetales Infections↗
PubMed1994

Induction of metallothionein synthesis by bismuth in cultured vascular endothelial cells.

Metallothionein synthesis induced by bismuth nitrate was characterized using a cell culture system. It was found that bismuth (1-10 microM) significantly increased the intracellular accumulation of metallothionein in bovine aortic endothelial cells without an exhibition of cytotoxicity and a change of either general protein synthesis or proliferative DNA synthesis after a 24-h incubation. A low increase in the metallothionein accumulation was observed in bovine aortic smooth muscle cells; however, porcine kidney epithelial LLC-PK1 cells, human Chang liver cells and two human hepatoma cell lines (HLF cells and Hep-G2 cells) did not respond to bismuth. Other cations including cobalt, lead and zinc at 10 microM failed to induce metallothionein in endothelial cells, although cadmium at 1 microM was a strong inducer. Bismuth accumulated highly in endothelial cells but very slightly in LLC-PK1 cells and Chang liver cells. The present data suggest that bismuth is a selective inducer of metallothionein of vascular endothelial cells and this cell type particularly responds to the cation.

Adenine↗
PubMed1993

Cadmium stimulation of plasminogen activator inhibitor-1 release from human vascular endothelial cells in culture.

We investigated the effect of cadmium (0.5, 1.0 or 2.0 microM) on the release of plasminogen activator inhibitor-1 antigen (PAI-1:Ag) from cultured human vascular endothelial cells. It was found that cadmium at 1.0 and 2.0 microM significantly increased the PAI-1:Ag release from the cells after a 24-h incubation. However, the tissue plasminogen activator antigen (t-PA:Ag) release was not changed by the metal. Although nickel as well as cadmium increased the PAI-1:Ag release, the other heavy metals including cobalt, zinc and copper did not exhibit such a stimulatory effect. The incorporation of [3H]leucine into the acid-insoluble fraction of the cell layer was unchanged by cadmium, suggesting that the metal may stimulate the synthesis of PAI-1 without association with generalized increase in protein synthesis. Cadmium at 1.0 and 2.0 microM significantly decreased the t-PA activity in the medium. The present study showed that cadmium increases the release of PAI-I:Ag from cultured endothelial cells without non-specific stimulation of protein synthesis. The decrease in the t-PA activity suggests an implication of cadmium in vascular lesion which is mediated by anti-fibrinolytic activity.

Cadmium↗
PubMed1993

Tumor necrosis factor alpha-induced alteration of glycosaminoglycans in cultured vascular smooth-muscle cells.

We studied alteration of glycosaminoglycans (GAGs) induced by recombinant human tumor necrosis factor alpha (rhTNF alpha) in vascular smooth-muscle cells from bovine aorta in a culture system. It was found that rhTNF alpha at 10 ng/ml and below significantly increased the incorporation of [35S]sulfate (35S) but conversely decreased that of [3H]glucosamine (3H) into GAGs in the trypsinate fraction of the cell layer after a 24-h incubation. These results suggested that rhTNF alpha reduced the formation and/or the anchorage of sugar chains in the cell layer but enhanced their sulfation in whole GAG synthesis by the cells. In results, the ratio of 35S to 3H in the GAGs was markedly increased. This increase occurred after 24 h and longer when the cells were treated with 1.0 ng/ml rhTNF alpha. The TNF alpha-induced alteration of the incorporation of both 35S and 3H was completely blocked by anti-rhTNF alpha antibody. Other cytokines including recombinant human interleukin-1 beta and -6, and platelet-derived growth factor failed to alter the ratio of 35S to 3H in the GAGs of the trypsinate fraction of the cell layer. In cultured vascular endothelial cells from bovine aorta, however, rhTNF alpha at 1.0 ng/ml significantly decreased the incorporation of both 35S and 3H into GAGs of both the trypsinate fraction and the medium; the ratio of 35S to 3H was not changed. Characterization of GAGs in vascular smooth muscle cell trypsinate fraction revealed that rhTNF alpha at 10 ng/ml induced (i) no change of the incorporation of 3H in the hyaluronate fraction, (ii) a marked increase in the incorporation of 35S and no change of that of 3H in chondroitin sulfates (A plus C) fraction, (iii) a significant decrease in the incorporation of both 35S and 3H in the heparan sulfate fraction, and (iv) no change of the incorporation of 35S and a marked decrease in that of 3H in the dermatan sulfate fraction. In the medium, rhTNF alpha also induced various changes of GAGs. It was therefore concluded that TNF alpha may have a capacity of inducing a qualitative change of vascular smooth-muscle cell GAGs, which may be involved in the vascular pathology such as atherosclerosis.

Animals↗
PubMed1993

Ano-urethral fistula, a special type of anomaly: report of two cases.

Two cases of an ano-urethral fistula, being a low malformation, are reported herein. Both patients underwent a colostomy under the diagnosis of a recto-urethral fistula during the neonatal period. As a urethro-rectogram later revealed the fistula to be located between the anus and anterior urethra, revision of the urethral fistula and an anoplasty were performed through the perineal approach. It is very difficult to establish a correct diagnosis of an ano-urethral fistula at the initial stage of treatment, but we found the urethro-rectogram invaluable in this regard. This type of malformation can be treated through the perineal approach, while the additional anterior perineal incision is very helpful for revising the urethral fistula.

Anal Canal↗
PubMed1993

Metallothionein induction by cadmium, cytokines, thrombin and endothelin-1 in cultured vascular endothelial cells.

Metallothionein induction was investigated using vascular endothelial cells derived from bovine aorta in a culture system. The induction occurred by cadmium (2 and 5 microM) but not by zinc (10 and 300 microM) after a 24-h incubation of the confluent cultures. It was revealed that cytokines including interleukin-1 beta, interleukin-6, tumor necrosis factor alpha and transforming growth factor beta (1 ng/ml each) have a capacity of metallothionein induction. In these inducers, only cadmium and tumor necrosis factor alpha exhibited significant cytotoxicity, suggesting that metallothionein is not induced simply in response to cytotoxicity. It was found that either thrombin or endothelin-1 which are coagulation factor or anti-fibrinolytic factor, respectively, also induced metallothionein synthesis. It was therefore suggested that metallothionein in endothelial cells may be involved in the regulation of the functions of these cells as well as the protection against cytotoxic agents.

Animals↗