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H Yamanishi

Publications and source records attributed to H Yamanishi.

13 recordsLinked to original sources
PubMed1992

Effects of prodigiosin 25-C on cultured cell lines: its similarity to monovalent polyether ionophores and vacuolar type H(+)-ATPase inhibitors.

Prodigiosin 25-C inhibited the proliferation of various cultured cell lines more strongly when concanavalin A (Con A) was added to the cultures. The increase in sensitivity was most evident in T lymphoma YAC-1 cells. The combination of prodigiosin 25-C and Con A induced characteristic morphological changes in these cells. In the presence of Con A, monovalent polyether ionophores and vacuolar type H(+)-ATPase inhibitors induced effects similar to those of prodigiosin 25-C on YAC-1 cells. Prodigiosin 25-C had neither K+ionophore activity nor inhibitory effect on vacuolar type H(+)-ATPase. A Golgi mannosidase II inhibitor, swainsonine, inhibited the proliferation of YAC-1 cells only when Con A was added. Prodigiosin 25-C and swainsonine increased Con A binding receptors on the surface of YAC-1 cells. These results suggest that prodigiosin 25-C affects the intracellular transport and/or processing of glycoproteins.

Biological Transport↗
PubMed1991

Proliferation of Shionogi carcinoma 115 cells by glucocorticoid-induced autocrine heparin-binding growth factor(s) in serum-free medium.

Shionogi carcinoma 115 (SC115) has been accepted for 20 years as an androgen-responsive mouse mammary tumor. Recently, the growth of the tumor was also found to be stimulated by pharmacological, but not physiological, doses of glucocorticoid. In a serum-free culture system [Ham's F-12:Eagle's minimal essential medium (1:1, v/v) containing 0.1% bovine serum albumin], we have established that 10(-8) M testosterone, or 10(-6) M dexamethasone significantly stimulates the growth of SC-3 cells (a cloned cell line from a SC115 tumor) via androgen and glucocorticoid receptors, respectively. Recently, we demonstrated that the testosterone-induced growth of SC-3 cells is mediated through autocrine fibroblast growth factor (FGF)-like peptide(s). In the present study, mechanisms of glucocorticoid-induced growth of SC-3 cells were investigated. Serum-free conditioned medium obtained from 10(-6) M dexamethasone-stimulated SC-3 cells was fractionated by heparin-Sepharose affinity chromatography; one sharp peak of growth-stimulatory activity for SC-3 cells, eluted at 1.3 M NaCl, was identified. When the peak fraction was added to serum-free medium, the shape of SC-3 cells changed from an epithelial to a fibroblast-like appearance, similar to that induced with testosterone or basic (b)FGF. Furthermore, the growth-stimulatory activity induced with the peak fraction as well as testosterone or bFGF was markedly inhibited by anti-bFGF antibody immunoglobulin G (75 to 90% inhibition was obtained), and the specific binding of 125I-bFGF on SC-3 cells was significantly inhibited by the peak fraction. These results suggest that the glucocorticoid-induced growth of SC-3 cells is also mediated through FGF-like peptide(s) in an autocrine mechanism, which is very similar to that induced by testosterone, if not identical.

Animals↗
PubMed1991

Heparin inhibits autocrine stimulation but not fibroblast growth factor stimulation of cell proliferation of androgen-responsive Shionogi carcinoma 115.

An androgen-responsive cloned cell line (SC-3) derived from Shionogi carcinoma 115 (SC115) has been shown to secrete fibroblast growth factor (FGF)-like peptide in response to androgen, which binds to FGF receptor and promotes the proliferation of SC-3 cells in an autocrine mechanism. Since the androgen-induced autocrine factor has a property to bind heparin, we examined the effects of heparin on the growth of SC-3 cells. Heparin was found to exhibit significant inhibition of testosterone-induced growth in a concentration-dependent manner: Approximately 50% inhibition was found at a concentration of 0.1 micrograms/ml. DNA synthesis of SC-3 cells induced by testosterone was also inhibited strongly by heparin, and less strongly by heparan sulfate and dermatan sulfate. Proliferation of SC-3 cells induced by acidic (a) or basic (b) FGF appeared not to be modulated by heparin. In contrast, heparin efficiently blocked DNA synthesis stimulated with androgen-induced growth factor in the conditioned medium from testosterone-treated cells. These results indicate that heparin inhibits autocrine loop in SC-3 cells induced by androgen. Thus, the autocrine growth factor possesses a different characteristic from aFGF and bFGF in that its bioactivities are negatively modulated by the glycosaminoglycan.

Animals↗
PubMed1990

Roles of transforming growth factor beta in inhibition of androgen-induced growth of Shionogi carcinoma cells in serum-free medium.

Shionogi carcinoma 115 (SC115) has been accepted for 20 years as an androgen-responsive mouse mammary tumor. In a serum-free culture system we have established [Ham's F-12:Eagle's minimum essential medium (1:1, v/v) containing 0.1% bovine serum albumin], 10(-8) M testosterone markedly stimulates the growth of SC-3 cells (a cloned cell line from a SC115 tumor) via androgen receptor. The testosterone-induced growth of SC-3 cells, which has been shown to be mediated through autocrine fibroblast growth factor (FGF)-like peptide, was almost completely abolished by 1 ng/ml of transforming growth factor beta (TGF-beta). In the present study, mechanisms of the inhibitory effect of TGF-beta on the testosterone-induced growth of SC-3 cells were examined in the serum-free medium. Although the testosterone-induced growth was almost completely inhibited by TGF-beta, basic FGF- or FGF-like peptide (secreted from SC-3 cells by testosterone)-induced growth was only partially inhibited (45%) by TGF-beta. This difference can be explained by the fact that TGF-beta decreased the amount of testosterone-induced FGF-like peptide secreted from SC-3 cells to 18% of control. The TGF-beta-induced inhibition was found to be reversible. Furthermore, no significant effects of the TGF-beta treatment on number or affinity of both androgen and FGF receptors were demonstrated. The present findings show that TGF-beta markedly inhibits testosterone-induced secretion of FGF-like peptide from SC-3 cells and also inhibits growth-stimulatory effects of the secreted factor on SC-3 cells, probably via postreceptor mechanisms.

Animals↗
PubMed1990

Interaction of androgen-induced autocrine heparin-binding growth factor with fibroblast growth factor receptor on androgen-dependent Shionogi carcinoma 115 cells.

Stimulation of a Shionogi carcinoma 115-derived cultured cell line (SC-3) with androgen resulted in secretion of heparin-binding growth factor. In this study, we analyzed cell-surfaced receptors for growth factors. Binding data of growth factors on intact SC-3 cells revealed the presence of low and high affinity receptors for epidermal growth factor (EGF), insulin, and fibroblast growth factor (FGF). The dissociation constant values were 50 pM and 1.0 nM for EGF, 1.2 nM and 30 nM for insulin, and 34 pM and 7.5 nM for FGF. The numbers of maximal binding sites were 300 and 900/cell for EGF, 2,000 and 14,000/cell for insulin, and 13,000 and 810,000/cell for FGF. To examine the association of androgen-induced growth factor with one of these receptors, the conditioned medium prepared from androgen-stimulated SC-3 cells was fractionated through a heparin-Sepharose column. Growth factor activity adsorbed and eluted by 1 M NaCl from the column was comigrated with the activity inhibiting FGF-receptor association. In addition, basic 125I-FGF was cross-linked, using disuccinimidyl suberate, to the receptor with an apparent molecular weight of 130,000, whose labeling was inhibited when basic FGF, acidic FGF, or highly purified androgen-induced growth factor was present in excess. Furthermore, the highly purified growth factor-, basic FGF- or androgen-induced growth of SC-3 cells was significantly and similarly inhibited by anti-basic FGF antibody IgG. These results indicate that androgen-induced FGF-like factor acts as an autocrine growth factor via the FGF receptor in a process of SC-3 cell proliferation.

Animals↗
PubMed1990

Growth stimulation by androgens, glucocorticoids or fibroblast growth factors and the blocking of the stimulated growth by antibody against basic fibroblast growth factor in protein-free culture of Shionogi carcinoma 115 cells.

Shionogi carcinoma 115 (SC115) has been accepted for 20 years as an androgen-responsive mouse mammary tumor. We have established an androgen-dependent cloned cell line (SC-3) from a SC115 tumor. In a serum-free medium, testosterone (T) or fibroblast growth factors (FGFs) markedly stimulate the growth of SC-3 cells, and the T-induced growth was shown to be mediated through FGF-like peptide(s) in an autocrine mechanism. Since we used the serum-free culture including 0.1% bovine serum albumin (BSA), a partially serum-containing condition, putative roles of BSA- or serum-borne growth factors in growth stimulation of autocrine production of FGF-like peptide(s) could not be excluded. This paper reports findings performed in a protein-free medium including plating [Ham's F-12:MEM (1:1; v/v)]. In the protein-free culture, the growth of SC-3 cells was significantly stimulated by the addition of greater than or equal to 10(-10) M T (up to 20-fold), greater than or equal to 10(-7) M dexamethasone (Dex; up to 7-fold) or greater than or equal to 1 ng/ml basic (b) or acidic FGF (up to 10-fold); other various growth factors had no such effects. Furthermore, DNA synthesis of SC-3 cells induced by T, Dex or bFGF was similarly and markedly inhibited by bFGF neutralizing antibody IgG. Therefore, the present findings seem to demonstrate that androgens or high levels of glucocorticoids induce the production and secretion of FGF-like peptide(s) from SC-3 cells for their growth even in the absence of additional support by other factors.

Androgens↗
PubMed1989

Inhibitory effect of antibody against basic fibroblast growth factor on androgen- or glucocorticoid-induced growth of Shionogi carcinoma 115 cells in serum-free culture.

Shionogi carcinoma 115 (SC115) has been accepted for 20 years as an androgen-responsive mouse mammary tumor. However, we and others recently found that the growth of SC115 cells is also stimulated by high doses of glucocorticoids. We already reported the following findings. In a serum-free medium [Ham's F-12: Eagle's minimum essential medium (1:1, v/v) containing 0.1% bovine serum albumin], greater than or equal to 10(-9) M testosterone and greater than or equal to 10(-8) M dexamethasone significantly stimulated the growth of SC-3 cells (a cloned cell line from a SC115 tumor) through androgen and glucocorticoid receptors, respectively. In the present study, we have demonstrated that higher concentrations (10(-7)-10(-6) M) of weak androgens such as 4-androstene-3,17-dione or weak glucocorticoids such as corticosterone also significantly stimulate the growth of SC-3 cells and that their relative potency is found to be in parallel with their binding affinity for their receptors, respectively. Furthermore, DNA synthesis of SC-3 cells induced by 0.1 ng/ml basic fibroblast growth factor (FGF), 10(-8) M testosterone, 10(-6) M 4-androstene-3,17-dione, 10(-7) M dexamethasone, or 10(-6) M corticosterone was found to be similarly and significantly inhibited by the addition of basic FGF neutralizing antibody IgG in the present study; approximately 70% inhibition of the basic FGF, androgen, or glucocorticoid effects was attained. We already reported findings which suggest that SC-3 cells produce FGF-like peptide for their testosterone-induced growth. Therefore, the present study presents new additive information to demonstrate that the growth-stimulatory activity of various androgens or possibly glucocorticoids on SC-3 cells is mediated through a FGF-like peptide in an autocrine mechanism.

Androstenedione↗
PubMed1989

Growth-stimulatory effects of androgen, high concentration of glucocorticoid or fibroblast growth factors on a cloned cell line from Shionogi carcinoma 115 cells in a serum-free medium.

The effects of various kinds of growth factors or steroids on the proliferation of Shionogi carcinoma 115 (SC115) cells were investigated in cell culture. In a serum-free medium [Ham's F-12:Eagle's minimum essential medium (1:1, vol/vol) containing 0.1% bovine serum albumin], the proliferation of SC-3 cells (a cloned cell line from SC115 cells) estimated by [3H]thymidine incorporation into DNA and cell number reached a plateau at 10(-8) M testosterone (up to 200-fold), 10(-7) M dexamethasone (up to 30-fold) or 1 ng/ml of fibroblast growth factors (FGF; up to 50-fold). However, the proliferation in the serum-free medium was not significantly stimulated by the addition of low to very high concentrations of progesterone, oestradiol-17 beta, epidermal growth factor, platelet derived growth factor or insulin; transforming growth factor beta slightly stimulated the growth (up to 5-fold) but markedly inhibited the growth stimulation induced by testosterone. Furthermore, an epithelial appearance of SC-3 cells grown in the absence of growth factors or steroids was changed to a fibroblast-like appearance only by the addition of testosterone, high concentrations of dexamethasone or FGF. By investigating various kinds of growth factors or steroids, the present study demonstrates that androgen, high concentration of glucocorticoid or FGF alone significantly stimulates the proliferation of SC-3 cells with a change of morphology in the serum-free medium.

Animals↗
PubMed1987

Partial characterization of a Hantavirus isolated from a Clethrionomys glareolus captured in Belgium.

A Hantavirus was isolated in Vero-E6 cells from lungs of a free living bank vole (Clethrionomys glareolus) captured in Turnhout, Province of Antwerp--Northern part of Belgium. With help of monoclonal antibodies the Belgian Hantavirus isolate could be clearly differentiated from Hantaan virus strain 76-118, Prospect Hill virus strain PH1 and SR11, a Hantavirus isolated from laboratory Wistar rat in Japan, but not from the nephropathia epidemica virus strain Hällnäs.

Animals↗
PubMed1976

The removal of non-collagen components from newborn calf dermis with magnesium chloride solution.

1. Non-collagenous substances in newborn calf dermis were extracted with solutions of various concentrations of MgCl2. The total protein and hydroxyproline contents in MgCl2 extracts increased with increase in the concentration of MgCl2 in the solutions. In particular, steep increases of their contents were observed at concentrations of MgCl2 from 0.5 to 1.0 M. Total amounts of hydroxyproline in 1.0, 2.0, and 3.0 M MgCl2 extracts were equivalent to 40-50% of the hydroxyproline content in the whole connective tissue. Hexose and hexosamine contents of MgCl2 extracts increased with increase of the MgCl2 concentration. Hexuronic acid was hardly present in the residues after extractions with 0.5, 1.0, 2.0, and 3.0 M MgCl2. 2. Plasma proteins, hyaluronic acid, and dermatan sulfate were extracted at low concentrations of MgCl2. A non-collagenous protein and MgCl2-soluble collagen were extracted with 1.0, 2.0, and 3.0 M MgCl2 solutions. The disperson of collagen fibrils was observed in the residue extracted with 1.0 M MgCl2 solution by electron microscopy; the fibril structure of collagen was disordered by extraction with 2.0 and 3.0 M MgCl2. The results suggest that the dispersion and disorder of collagen fibrils lead to the release of a non-collagenous protein. Furthermore, it is suggested that the removal of hyaluronic acid and dermatan sulfate was not very effective for the solubilization of a large amount of collagen, but was suitable as a pretreatment to the extraction of a non-collagenous protein accompanied by the solubilization of a large amount of collagen. 3. The non-collagenous protein was purified by DEAE-cellulose column chromatography. Polyacrylamide gel electrophoresis of this protein at pH 8.5 showed a single band moving to the cathode. The non-collagenous protein contained 3.7% hexose, 1.8% hexosamine, and no hexuronic acid. This protein is rich in glycine, glutamic acid, and alanine, and contains neither hydroxyproline nor hydroxylysine. Sedimentation analysis showed a single peak with 1.8 S and the molecular weight was approx. 43,000 as determided by SDS polyacrylamide gel electrophoresis.

Amino Acids↗
PubMedDate not supplied

Effects of various growth factors on growth of a cloned human esophageal squamous cancer cell line in a protein-free medium.

In order to investigate molecular mechanisms of the growth of human esophageal cancer in relation to growth factors, we have recently established a protein-free culture system [Ham's F-12: Eagle's minimum essential medium (1:1, v/v)] of TE-3-OS cells (a cloned cell line from human esophageal squamous cancer, TE-3). In the present study, we first examined effects of exogenous growth factors on the growth of TE-3-OS cells. The growth of TE-3-OS cells in the protein-free medium was significantly stimulated by insulin and insulin-like growth factor (IGF)-I or IGF-II, and less effectively stimulated by epidermal growth factor (EGF) or transforming growth factor (TGF)-alpha; platelet-derived growth factor, TFG-beta, acidic fibroblast growth factor (FGF) or basic FGF had no effects. TE-3-OS cells contained specific IGF-I binding sites (110,000 sites/cell), with a Kd value of 800 pM. Moreover, the growth induced by IGF-I, IGF-II or insulin was markedly and similarly (70-80%) inhibited by anti-IGF-I receptor antibody IgG. These data suggest that IGF-I, IGF-II and insulin, as well as EGF and TGF-alpha, are important mitogens for human esophageal cancer cells and that effects of IGFs and insulin are mediated predominantly via IGF-I receptors.

Carcinoma, Squamous Cell↗
PubMedDate not supplied

Effects of androgen, fibroblast growth factors or other various growth factors on growth of Shionogi carcinoma cells in a protein-free medium.

Shionogi carcinoma 115 (SC115) has been accepted for 20 years as an androgen-responsive mouse mammary tumor. We have recently established an androgen-dependent cloned cell line (SC-3) from a SC115 tumor. We found in the present study that the growth of SC-3 cells can be stimulated by 10(-8) M testosterone (up to 100-fold) even in a protein-free medium beginning from plating [Ham's F-12: Eagle's minimum essential medium (1:1, v/v)]. In the protein-free culture, the proliferation of SC-3 cells was also found to be stimulated by acidic or basic fibroblast growth factor (FGF) alone (up to 50-fold) among various growth factors examined such as FGFs, insulin, insulin-like growth factor (IGF)-I, IGF-II, nerve growth factor, platelet-derived growth factor, epidermal growth factor, transforming growth factor (TGF)-alpha and TGF-beta. The testosterone (10(-8) M)- or FGF (10 ng/ml)-induced growth of SC-3 cells was abolished only by TGF-beta (greater than or equal to 1 ng/ml) among various growth factors examined. We show for the first time in this study an androgen-dependent growth of cancer cells (SC-3) in a protein-free medium. In the protein-free medium, growth of SC-3 cells is also stimulated by FGFs, and the androgen- or FGF-induced growth is inhibited only by TGF-beta.

Animals↗