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T Suda

Publications and source records attributed to T Suda.

At least 559 records · Page 31Linked to original sources
PubMed1991

Transglutaminase is involved in the fusion of mouse alveolar macrophages induced by 1 alpha, 25-dihydroxyvitamin D3.

We have reported that 1 alpha,25-dihydroxyvitamin D3 [1 alpha, 25(OH)2D3] induces fusion of mouse alveolar macrophages directly by a mechanism involving spermidine-dependent protein synthesis (Tanaka, H. et. al., 1989, Exp. Cell Res. 180, 72-83). The macrophage fusion induced by 1 alpha,25(OH)2D3 occurred in a calcium-dependent manner (Jin, C.H. et al., 1988, J. Cell. Physiol. 137, 110-116). In the present study, we examined the possibility that transglutaminase, a calcium-dependent enzyme, is involved in the fusion of macrophages induced by 1 alpha,25(OH)2D3. The activity of transglutaminase increased greatly 12 h after 1 alpha,25(OH)2D3 was ended and reached a maximum at 48 h. Western blot analysis of the cell lysate using an anti-transglutaminase antibody showed that 1 alpha,25(OH)2D3 induced a 77-kDa protein corresponding to transglutaminase. When spermidine synthesis was inhibited by adding methylglyoxal bis(guanylhydrazone) (MGBG), an inhibitor of S-adenosylmethionine decarboxylase, the increase in the transglutaminase synthesis by 1 alpha,25(OH)2D3 was markedly inhibited with concomitant inhibition of fusion. Adding more spermidine restored both the synthesis of transglutaminase and the fusion. The treatment of macrophages with cystamine, an inhibitor of transglutaminase, inhibited the fusion in parallel with the suppression of transglutaminase activity, both induced by 1 alpha,25(OH)2D3. These results clearly indicate that 1 alpha,25(OH)2D3 induces transglutaminase by a spermidine-dependent mechanism and that this enzyme is involved in a biological reaction(s) essential for inducing macrophage fusion.

Animals↗
PubMed1991

Putrescine is involved in the vitamin D action in chick intestine.

We have reported that a single injection of 1 alpha,25-dihydroxyvitamin D3 into vitamin D-deficient chicks produces a marked increase of putrescine accumulation in the duodenum from two different sources, ornithine and spermidine. In the present study, the effects of putrescine depletion and its supplementation on duodenal villus length and calcium absorption were examined in newborn and 5-week-old chicks. Administering either alpha-difluoromethylornithine, a specific inhibitor of ornithine decarboxylase, or N1,N4-bis(2,3-butadienyl)-1,4-butanediamine, a specific inhibitor of polyamine oxidase, to newborn chicks significantly decreased the duodenal content of putrescine and calcium transport activity. The putrescine depletion also induced shortening of the duodenal villus length. The inhibition of calcium absorption and villus length in the putrescine-depleted chicks was almost completely restored by administering putrescine to the birds. The effect of the putrescine depletion and its supplementation on the duodenal villus length and the calcium absorption was reproduced in 5-week-old vitamin D-deficient chicks given vitamin D3 or 1 alpha,25-dihydroxyvitamin D3. These results clearly indicate that putrescine is somehow involved in the vitamin D action in maintaining the morphological and functional development of the intestinal villus mucosa.

Acetyltransferases↗
PubMed1991

A stable analogue of thromboxane A2, 9,11-epithio-11,12-methanothromboxane A2, stimulates bone resorption in vitro and osteoclast-like cell formation in mouse marrow culture.

Thromboxane A2 (TXA2) is a powerful promoter of platelet aggregation and smooth muscle contraction. However, this compound is highly unstable and is rapidly hydrated to a more stable metabolite, thromboxane B2 (TXB2). TXA2 has been considered to be involved in bone resorption, in particular bone loss caused by inflammatory diseases and by orthodontic treatment. However precise mechanisms of bone resorption caused by TXA2 have not yet been proved because of its highly unstable nature. Recently, a chemically stable analogue of TXA2, 9,11-epithio-11,12-methanothromboxane A2 (STA2), was successfully synthesized. Using this synthetic compound, we examined its in vitro bone resorbing activity and induction of osteoclast-like cells in a mouse marrow culture system in comparison with related compounds with bone resorbing activity. Like prostaglandin E2 (PGE2), a well-known bone resorbing agent, STA2 time- and dose-dependently stimulated the release of 45Ca from prelabelled mouse calvariae. Both STA2 and PGE2 induced the accumulation of cAMP in mouse calvariae. The TXA2 antagonist, ONO-3708, inhibited STA2-induced release of 45Ca. TXB2 induced neither bone resorption nor cAMP accumulation. When mouse marrow cells were cultured with STA2 for 8 days, osteoclast-like multinucleated cells appeared in parallel with the increase of the amount of STA2 added. Again TXB2 showed no effect on osteoclast-like cell formation. These results indicate a role for TXA2 in some form of bone resorption.

Animals↗
PubMed1991

Recombinant human bone morphogenetic protein-2 stimulates osteoblastic maturation and inhibits myogenic differentiation in vitro.

The in vitro effect of recombinant human bone morphogenetic protein-2 (rhBMP-2) on osteogenic and myogenic differentiation was examined in two clonal cell lines of rat osteoblast-like cells at different differentiation stages, ROB-C26 (C26) and ROB-C20 (C20). The C26 is a potential osteoblast precursor cell line that is also capable of differentiating into muscle cells and adipocytes; the C20 is a more differentiated osteoblastic cell line. Proliferation was stimulated by rhBMP-2 in C26 cells, but inhibited in C20 cells. rhBMP-2 greatly increased alkaline phosphate (ALP) activity in C26 cells, but not in C20 cells. The steady-state level of ALP mRNA was also increased by rhBMP-2 in C26 cells, but not in C20 cells. Production of 3',5'-cAMP in response to parathyroid hormone (PTH) was dose-dependently enhanced by adding rhBMP-2 in both C26 and C20 cells, though the stimulatory effect was much greater in the former. There was neither basal expression of osteocalcin mRNA nor its protein synthesis in C26 cells, but they were strikingly induced by rhBMP-2 in the presence of 1 alpha,25-dihydroxyvitamin D3. rhBMP-2 induced no appreciable changes in procollagen mRNA levels of type I and type III in the two cell lines. Differentiation of C26 cells into myotubes was greatly inhibited by adding rhBMP-2. The inhibitory effect of rhBMP-2 on myogenic differentiation was also observed in clonal rat skeletal myoblasts (L6). Like BMP-2, TGF-beta 1 inhibited myogenic differentiation. However, unlike BMP-2, TGF-beta 1 decreased ALP activity in both C26 and C20 cells. TGF-beta 1 induced neither PTH responsiveness nor osteocalcin production in C26 cells, but it increased PTH responsiveness in C20 cells. These results clearly indicate that rhBMP-2 is involved, at least in vitro, not only in inducing differentiation of osteoblast precursor cells into more mature osteoblast-like cells, but also in inhibiting myogenic differentiation.

Alkaline Phosphatase↗
PubMed1991

Generation of B lymphocytes from a single hemopoietic progenitor cell in vitro.

The first stages of the pathway by which lymphocytes differentiate from hemopoietic stem cells were studied at a clonal level. When 211 interleukin 3 (IL-3)-induced blast colonies shown to be capable of differentiating into a variety of hemopoietic cells were individually transferred into wells containing a monolayer of stromal cells, growth in granulocyte, macrophage, megakaryocyte, or mast cell lineages was observed in 192 wells. In seven of these 192 wells, lymphoid cell growth also was seen. The lymphoid cells were proved to be B lymphocytes by phenotype and immunoglobulin gene rearrangement analyses and by demonstration of surface expression of IgM. The clonal origin of myeloid and B lymphocyte lineage cells was further confirmed by the generation of both myeloid and B lymphoid cells in the same well following FACS clone-sorting of IL-3 induced blast cells. These results provide in vitro evidence that cells of B lymphoid and myeloid lineage can originate clonally from single primitive hemopoietic stem cells.

Animals↗
PubMed1991

Multipotent and committed CD34+ cells in bone marrow transplantation.

In order to study the role of CD34+ cells in hematological recovery following bone marrow transplantation (BMT), bone marrow cells stained with HPCA-1 (CD34) and MY-9 (CD33) monoclonal antibodies were analyzed by using a fluorescence-activated cell sorter on or about days 14 and 28, as well as at later times, following BMT in 6 recipients. Single cell cultures of CD34+ cells were also performed to evaluate their in vitro hematopoietic function. CD34+ cells were detectable in bone marrow cells on day 14. More than 80% of CD34+ cells co-expressed the CD33 antigen, and macrophage (Mac) colony-forming cells predominated among total colony-forming cells of CD34+ cells. In normal bone marrow cells, CD34+, CD33+ cells amounted to about 40% of CD34+ cells, and the incidences of erythroid bursts, granulocyte/macrophage (GM) colonies, and Mac colonies were similar to each other. After more than 10 weeks, CD34+, CD33- cells gradually recovered, as erythroid burst colony-forming cells increased following GM colony-forming cells. This phenomenon was well-correlated with the time course of peripheral blood cell recovery. CD34+, CD33+ cells as committed progenitors and CD34+, CD33- cells as multipotent stem cells have distinctive biological behaviors in BMT.

Antibodies, Monoclonal↗
PubMed1991

Long-term effects of ofloxacin on clinical courses in patients with diffuse panbronchiolitis.

To ascertain the long-term effects of ofloxacin (OFX) on clinical parameters in cases of diffuse panbronchiolitis (DPB), we treated 18 patients with this disease with OFX and compared the clinical findings before and after treatment. Pulmonary function tests including percent vital capacity, arterial oxygen tension and arterial-alveolar oxygen tension difference significantly improved with OFX. In addition, the incidence of acute exacerbation and the duration of hospitalization were reduced. These observations indicate that OFX is a useful drug for the management of chronic respiratory infections such as DPB.

Bronchiolitis↗
PubMed1991

Deficiency of osteoclasts in osteopetrotic mice is due to a defect in the local microenvironment provided by osteoblastic cells.

We have reported that osteoblastic cells are required for differentiation of osteoclast progenitors in splenic tissues into multinucleated osteoclasts. In the present study we examined the pathogenesis of the osteoclast deficiency in osteopetrotic (op/op) mice using a coculture system of spleen cells and osteoblastic cells. When spleen cells obtained from op/op or normal (+/?) littermates of op/+ parent mice were cocultured with osteoblastic cells obtained from calvaria of normal ddy strain mice, numerous tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells (MNCs) were formed in the presence of 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3]. Most of the TRAP-positive MNCs bound [125I]salmon calcitonin. This suggests that there is no abnormality in the osteoclast progenitors present in the splenic tissues of op/op mice. When osteoblastic cells from +/? littermates were cocultured with normal spleen cells from ddy mice, TRAP-positive MNCs were similarly formed in response to 1 alpha,25(OH)2D3. In contrast, in cocultures of op/op osteoblastic cells with normal spleen cells, no TRAP-positive cells appeared, even in the presence of 1 alpha,25(OH)2D3. The op/op mutation was recently reported to exist in the coding region of the macrophage colony-stimulating factor (M-CSF) gene. Adding M-CSF and 1 alpha,25(OH)2D3 to the coculture with op/op osteoblastic cells induced the appearance of TRAP-positive MNCs with calcitonin receptors. These results clearly indicate that osteoclast deficiency in op/op mice is due to a defect in the local microenvironment in bone, in which M-CSF produced by osteoblastic cells plays a critical role in osteoclast development.

Acid Phosphatase↗
PubMed1991

Angiotensin II increases the corticotropin-releasing factor messenger ribonucleic acid level in the rat hypothalamus.

Angiotensin II (AII) has an important role in the regulation of CRF release. In the present study, the effect of centrally administered AII on CRF messenger RNA (mRNA) levels in the rat hypothalamus was examined. Administration of 0.1 nmol and 1 nmol AII into the lateral ventricle increased the levels of plasma ACTH 20 min and 45 min after administration and those of proopiomelanocortin mRNA in the anterior pituitary (AP) and CRF mRNA in the hypothalamus 2 h after administration. On the other hand, ACTH levels in AP and CRF levels in the median eminence temporarily decreased 45 min after the administration of 1 nmol AII, but it returned to the control level at 90 min. Administration of 10 nmol saralacin, an AII antagonist, blocked 1 nmol AII-induced increase in the levels of plasma ACTH, proopiomelanocortin mRNA in AP, and CRF mRNA in the hypothalamus. These results indicate that central administration of AII increases the CRF mRNA level in the hypothalamus in a receptor-specific manner and also increases CRF release. Therefore, AII seems to have an important role in the regulation of the release and synthesis of CRF in the hypothalamus.

Adrenocorticotropic Hormone↗
PubMed1991

Transcriptional regulation of the production of the third component of complement (C3) by 1 alpha,25-dihydroxyvitamin D3 in mouse marrow-derived stromal cells (ST2) and primary osteoblastic cells.

We have purified a 190-kDa protein produced by mouse marrow-derived stromal cells (ST2) in response to 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25-(OH)2D3] and unequivocally identified it as mouse complement C3 (C3). In this study we examined the regulation by 1 alpha,25-(OH)2D3 of C3 production in ST2 cells at both the transcriptional and translational levels. 1 alpha,25-(OH)2D3 greatly increased the protein production of C3 at 24 h, and it attained a maximum at 72 h. C3 mRNA stimulation by 1 alpha,25-(OH)2D3 was initiated at 12 h and reached a maximum at 48 h. 1 alpha,25-(OH)2D3 increased the expression of C3 mRNA dose-dependently, ranging from 10(-10)-10(-8) M. The increase in the C3 production in response to 1 alpha,25-(OH)2D3 appeared to occur at a transcriptional level, since actinomycin-D completely inhibited both mRNA expression and protein production of C3 induced by 1 alpha,25-(OH)2D3. Besides 1 alpha,25-(OH)2D3, local bone-resorbing agents, such as interleukin-1 alpha, tumor necrosis factor-alpha, and lipopolysaccharides, also stimulated the expression of C3 mRNA, not only in ST2 cells, but also in primary osteoblastic cells. C3 production by hepatocytes occurred regardless of the presence or absence of 1 alpha,25-(OH)2D3. These results clearly indicate that 1 alpha,25-(OH)2D3 tissue-specifically regulates the synthesis of C3 in bone. Bone C3 may play an important role in bone metabolism.

Animals↗
PubMed1991

Presence of CRH-binding protein in amniotic fluid and in umbilical cord plasma.

CRH-binding protein was present in the amniotic fluid and in the umbilical cord plasma after 15 weeks and 24 weeks of pregnancy, respectively. The size of the CRH-binding protein was similar to that in the peripheral blood from normal subjects. The level of the binding of CRH-binding protein in the umbilical cord plasma during the third trimester of pregnancy was also similar to that in the peripheral blood of neonates and normal adult subjects. The binding of CRH-binding protein was temporarily decreased at 40 weeks of pregnancy. These results indicate that fetal CRH-binding protein seems to be produced at least in the second trimester of pregnancy.

Amniotic Fluid↗
PubMed1991

Morphological studies of the association of mitochondria with chlamydial inclusions and the fusion of chlamydial inclusions.

The association of mitochondria with the inclusions of five strains of Chlamydia psittaci, two strains of C. trachomatis and one strain of C. pneumoniae was examined by electron microscopy. The results demonstrated that mitochondrial association occurred only with the C. psittaci inclusions, but not with the C. trachomatis and C. pneumoniae inclusions. Multiple inclusions formed by infection with a single strain could fuse with each other during their expansion, but fusion never occurred between the C. trachomatis and C. psittaci inclusions as a result of dual infection with these different species.

Cell Nucleus↗
PubMed1991

Effects of interleukin 3, interleukin 6, and granulocyte colony-stimulating factor on sorted murine splenic progenitor cells.

In order to examine the effect of recombinant growth factors on hemopoietic stem cells, these cells were enriched using wheat germ agglutinin (WGA) and monoclonal antibodies for lineage markers (Lin) such as B220, L3T4, Lyt-2, asialo GM1, Mac-1, and AL-21. Spleen colony-forming units (CFU-S) and in vitro colony-forming units were highly enriched in the fraction of WGA+Lin- spleen cells. To eliminate committed progenitor cells, spleen cells of 5-fluorouracil (5-FU)-treated mice were used. By this treatment, day-8 CFU-S disappeared but day-14 CFU-S were preserved. Day-14 CFU-S were also contained in the fraction of WGA+Lin- cells, which made up about 0.5% of total nucleated spleen cells. Moreover, this fraction contained primitive stem cells that could reconstitute the hemopoiesis of irradiated mice. Sorted WGA+Lin- spleen cells obtained from male 5-FU-treated mice were injected into lethally irradiated female mice. Southern hybridization using a mouse Y chromosome-specific probe showed that the bone marrow, spleen, and thymus of the recipients was reconstituted by male mouse-derived cells. When sorted WGA+Lin- spleen cells of the 5-FU-treated mice were cultured in vitro in the presence of recombinant interleukin 3 (IL-3), interleukin 6 (IL-6), and granulocyte colony-stimulating factor (G-CSF), colony formation was observed only in wells with IL-3, whereas unfractionated spleen cells formed colonies in the presence of IL-3, IL-6, or G-CSF. However, IL-6 but not G-CSF acted synergistically on enriched hemopoietic stem cells in the presence of IL-3. These data suggest that G-CSF or IL-6 did not affect primitive stem cells independently but showed the effect on these cells indirectly or synergistically with IL-3.

Animals↗
PubMed1991

Factor with erythroid burst-promoting activity in human urine unlike other hematopoietic growth factors.

A factor with burst-promoting activity (BPA) stimulates the formation of erythroid bursts in the presence of erythropoietin, acting on early erythroid progenitor cells (erythroid burst-forming units, or BFU-E). Here we investigated the biological properties of this factor partially purified from the urine of anemic patients. The human urinary factor did not cause the formation of late erythroid progenitor cells (erythroid colony-forming units, or CFU-E) or enhance such colony formation in the presence of erythropoietin. Thus, the urinary factor was a different substance from erythroid potentiating activity and from activin, which act on both BFU-E and CFU-E. The urinary factor promoted the colony formation of BFU-E from both humans and mice, but the human hematopoietic growth factors such as recombinant interleukin-3, interleukin-6, granulocyte-macrophage colony-stimulating factor, and macrophage colony-stimulating factor did not stimulate the formation of BFU-E derived colonies from mice. The results suggested that the factor in the urine of anemic patients was different from the hematopoietic growth factors identified so far.

Anemia↗
PubMed1991

Long-term bone marrow failure accompanied by skin pigmentation.

A rare case of long-term bone marrow failure with skin pigmentation is presented. The patient was a female with a long history of anemia and skin pigmentation since childhood, although she had no malformations nor chromosomal abnormalities. Hematological improvement has been maintained by the administration of prednisolone. This case may differ from other disorders known as congenital aplastic anemia.

Addison Disease↗
PubMed1991

Immunoelectron microscopy of Fc receptors on the surface of clinical isolates of streptococci.

The distribution of Fc receptors on the surface of clinical isolates of streptococci was examined by immunoelectron microscopy. A unique two-layered ferritin tagging was observed on the surface of isolate MS-4 (group A). The spacing between the layers (10-40 nm) was narrower than that of the layered protein A (30-70 nm) on Staphylococcus aureus. Labeling on the other isolates, IP-28 (group A) and ES-21L (group C), showed similar rough layers, but the labeling were clearly different in thickness and density. The labeling on isolate IP-28 was also similar to that on strain AR1 (group A), reported previously, while the labeling on ES-21L was similar to that on protein G producing strain G148 (group G) in thickness. However, it was obviously thinner than that on IP-28 and AR1. These results strongly suggest that there are at least three distribution patterns of Fc receptors on streptococci, and these are distinct from that of protein A.

Hemagglutination Tests↗