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Volume 24 (1999)
- Issue 6 Pages 425-
- Issue 5 Pages 237-
- Issue 4 Pages 171-
- Issue 3 Pages 111-
- Issue 2 Pages 59-
- Issue 1 Pages 1-
Volume 24, Issue 3
Displaying 1-7 of 7 articles from this issue
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Tomokazu Matsuura, Satoshi Hasumura, Kazuhiro Nagamori1999 Volume 24 Issue 3 Pages 111-116
Published: 1999
Released on J-STAGE: March 27, 2000
JOURNAL FREE ACCESSThe mechanisms of retinol transport and Accumulation in hepatic stellate cells (HSC) remain to be clucidated. Our previous studies suggested that retinol esterfication activity, particularly lecithin: retinol acyltransferase (LRAT) activity, in liver retinoid metabolism is important to elucidate the relationship between retinol uptake by HSC and the esterification of retinol. In the present study, using a human HSC-like cell line, LI90, we demonstrated that retinol esterification activity of LI90, we demonstrated that retinol esterification activity of LI90 cells is similar to that of primary cultures of rat HSC and higher than that of a human hepatoma cell line. Further, since progesterone or diphos-pho-lauroyl-phosphatidylcholine increased retinol esterification activity of LI90 cells, it is likely that LRAT contributes to retinol esterification in LI90. We examined retinol esterification in LI90 cells and clearance of retinol from culture medium. The percentages of both retinol and esterified retinol in LI90 cells increased in a manner dependent of retinol concentration in medium, whereas that of retinol in medium decreased. The percentages of esterified and unesterified retinol in LI90 cells and of retinol in medium were linearly dependent on the logarithm of the initial concentration of retinol in the medium. These results suggest that retinol esterification activity contributes to retinol uptake by HSC and maintenance of non-toxic retinol levels in plasma.View full abstractDownload PDF (852K) -
Shoji Okamura, Koichi Okahara, Takayuki Iida, Miwa Ozaki, Sayaka Asano ...1999 Volume 24 Issue 3 Pages 117-122
Published: 1999
Released on J-STAGE: March 27, 2000
JOURNAL FREE ACCESSThe 3’-ends of the β-tubulin cDNA were amplified from tobacco BY2 polyA+ RNA. According to the differences in the predicted amino acid sequence at the extreme C-terminal, they were grouped into three different isotypes, NTB1 in which “EEGDYYEEDEEDLNEA”, NTB2 in which “EEEYYEDEEEAQED” and NTB3 in which “DECEYEEEEEYDHEGN” follows the conservative “YQQYQDATAD” sequence. Using unique 3’-untranslated regions as probes, changes in the RNA levels of each β-tubulin isotype were determined by dot-blot hybridization. The levels exhibited characteristic rhythms in the cell cycle. NTB1RNA was highest in S phase in comparison to NTB2 RNA level which was highest in late G2. On the other hand, NTB3 RNA level was highest in early G2.View full abstractDownload PDF (470K) -
Toshihiro Hata, Nobuyuki Yamaguchi, Yoshimasa Tanaka, Hideko Urushihar ...1999 Volume 24 Issue 3 Pages 123-129
Published: 1999
Released on J-STAGE: March 27, 2000
JOURNAL FREE ACCESSThe cellular slime mold Dictyostelium discoideum reproduces sexually under submerged and dark conditions. Its mating system is polymorphic and particularly interesting with respect to mechanisms of cell recognition. The cell-surface glycoprotein gp138 has been implicated in sexual cell interactions, as it was identified as a target molecule for the antibodies that block sexual cell fusion in D. discoideum. Two mutually homologous genes, GP138A and GP138B, have been cloned, but gene disruption experiments to clarify their functional relationships suggested that there is at least one more gene for gp138. Further protein analysis including peptide mapping also revealed that gp138 exists as three isoforms, DdFRP1, DdFRP2, and DdFRP3. GP138A encodes DdFRP2 and GP138B, DdFRP3, and the presence of a third gp138 gene encoding DdFRP1 was suggested. Here, we isolated and characterized a third GP138 gene, GP138C. Although the deduced amino acid sequences of GP138C matched completely with those of peptide fragments of DdFRP1 in the N-terminal half, the rest did not give complete matches. Overexpression of GP138C caused an increase in the intensity of DdFRP1, but disruption of this gene did not diminish DdFRP1. Our results indicate that GP138C encodes a protein very similar to but distinct from DdFRP1. The GP138 multigene family is thus composed of more members than previously expected, and their functional relationships are of special interest.View full abstractDownload PDF (564K) -
Mutsuko Takano, Teruo Shimmen1999 Volume 24 Issue 3 Pages 131-137
Published: 1999
Released on J-STAGE: March 27, 2000
JOURNAL FREE ACCESSTo study the mechanism of aluminum toxicity in plant cells, the effects of aluminum on alkaline band formation were analyzed in the internodal cells of Chara. After cells were treated with AlCl3, they were examined for their capacity to develop alkaline bands. Treating cells with AlCl3 medium at pH 4.5 completely inhibited alkaline band formation. When either CaCl2 or malic acid was added to the AlCl3 medium(pH 4.5), it did not produce an ameliorative effect, whereas addition of both CaCl2 and malic acid induced a significant ameliorative effect. It was found that treatment at pH 4.5 in the absence of AlCl3 strongly inhibited alkaline band formation. This inhibition by the low pH(4.5) treatment was effectively ameliorated by CaCl2. At higher pH(5.0), malic acid alone produced a significant ameliorative effect on aluminum inhibition of alkaline band formation, but CaCl2 did not. Recovery from aluminum inhibition was also studied. When cells treated with AlCl3 at pH 4.5 were incubated in artificial pond water, they could not recover the capacity to develop alkaline band. When either malic acid or CaCl2 was added to artificial pond water, cells recovered their alkaline band formation. It was concluded that one of the primary targets of aluminum is the plasma membrane and that aluminum affects the plasma membrane from the cell exterior at the beginning of the treatment(within 24 h). It was also suggested that the aluminum treatment impairs the HCO3- influx mechanism but not the OH- efflux mechanism.View full abstractDownload PDF (864K) -
Maria de Nazare C. Soeiro, Mauricio M. Paiva, Helene S. Barbosa, Maria ...1999 Volume 24 Issue 3 Pages 139-149
Published: 1999
Released on J-STAGE: March 27, 2000
JOURNAL FREE ACCESSMannosyl binding sites were detected “in vitro” on cardiomyocytes (CM) surface using horse-radish peroxidase (HRP) as the ligand. Binding assays revealed a specific recognition system, which was time-and concentration-dependent. The binding required physiological pH and was inhibited by EDTA and trypsin treatments. HRP binding was reduced by pre-incubations with low concentrations of D-mannose. Ultrastructural analysis of the endocytic process was followed using HRP coupled to colloidal gold particles (HRP-Au). The tracer was found within caveolae characterizing early steps of the receptor-mediated endocytosis. The addition of 10 mM D-mannose to the interaction medium blocked Trypanosoma cruzi uptake by CM. The labeling of CM with a subsaturating concentration of HRP-Au before their infection showed, by ultrastructural studies, that its association with trypomastigote forms occurred frequently near to HRP-gold particles that could also be seen to comprise the parasitophorous vacuole. After infection of CM with T. cruzi, a considerable reduction on HRP binding was noticed. Binding was almost completely restored by treating the infected cultures with the trypanocidal drug Nifurtimox. Our“in vitro” findings suggest that cardiomyocyte's mannose receptors localized at the sarcolemma mediates T. cruzi recognition and can be down-modulated by parasite infection.View full abstractDownload PDF (1419K) -
Yuko Inazawa, Shin Yonehara1999 Volume 24 Issue 3 Pages 151-159
Published: 1999
Released on J-STAGE: March 27, 2000
JOURNAL FREE ACCESSA single administration of agonistic anti-Fas mAb RK8 into mice decreased the number of bone marrow cells especially Mac1+ and Gr1+ Cells of myeloid lineage. These cells, which were shown to be Fas-positive in normal bone marrow, were directly eliminated in vivo by Fas-mediated apoptosis. After the elimination of Fas-positive bone marrow cells, bone marrow was reconstituted by successive increase of numbers of Grllow and Macllow myeloid precursor cells expressing high levels of Fas, which are minor constituents in normal bone marrow. The increased cells consisted at least two compotents, Grldull Macl+ cKit+ cells and Grlintermediated Macl+ cKit- cells, both of which were shown to be sensitive to Fas-induced apoptosis in vivo. Thus, Fas is functional in normal bone marrow and Fas-induced apoptosis in bone marrow enhances marked proliferation of Fas-expressing myeloid precursor cells in vivo.View full abstractDownload PDF (768K) -
Shohei Okada, Munehisa Yabuki, Tomoko Kanno, Keisuke Hamazaki, Tamotsu ...1999 Volume 24 Issue 3 Pages 161-168
Published: 1999
Released on J-STAGE: March 27, 2000
JOURNAL FREE ACCESSGeranylgeranylacetone (GGA) induces apoptosis in human leukemia HL-60 cells in a dose-and time-dependent manner. This effect was completely prevented by the pan-caspase inhibitor z-Val-Ala-Asp(OMe) fluoromethylketone, thereby implicating the caspase cascade in the process. Prior to DNA fragmentation, GGA treatment markedly activated caspase-3(-like) proteases, which might be responsible for the observed apoptosis. In addition, GGA treatment interfered with the processing and membrane localization of Rap1 and Ras, and these changes may be a result of apoptosis. Moreover, nitric oxide donors significantly accentuated the GGA-induced apoptosis, suggesting that the apoptotic pathway induced by GGA might be regulated by a redox-sensitive mechanism. Taken together, these data suggest that the isoprenoid, GGA, is an effective inducer of apoptotic cell death in HL-60 cells.View full abstractDownload PDF (547K)
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