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1.
Exp. mol. med ; Exp. mol. med;: 550-560, 2011.
Article de Anglais | WPRIM | ID: wpr-131297

RÉSUMÉ

Protein arginine methylation is important for a variety of cellular processes including transcriptional regulation, mRNA splicing, DNA repair, nuclear/cytoplasmic shuttling and various signal transduction pathways. However, the role of arginine methylation in protein biosynthesis and the extracellular signals that control arginine methylation are not fully understood. Basic fibroblast growth factor (bFGF) has been identified as a potent stimulator of myofibroblast dedifferentiation into fibroblasts. We demonstrated that symmetric arginine dimethylation of eukaryotic elongation factor 2 (eEF2) is induced by bFGF without the change in the expression level of eEF2 in mouse embryo fibroblast NIH3T3 cells. The eEF2 methylation is preceded by ras-raf-mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK1/2)-p21(Cip/WAF1) activation, and suppressed by the mitogen-activated protein kinase (MAPK) inhibitor PD98059 and p21(Cip/WAF1) short interfering RNA (siRNA). We determined that protein arginine methyltransferase 7 (PRMT7) is responsible for the methylation, and that PRMT5 acts as a coordinator. Collectively, we demonstrated that eEF2, a key factor involved in protein translational elongation is symmetrically arginine-methylated in a reversible manner, being regulated by bFGF through MAPK signaling pathway.


Sujet(s)
Animaux , Souris , Arginine , Dédifférenciation cellulaire , Inhibiteur p21 de kinase cycline-dépendante/génétique , Elongation Factor 2 Kinase/métabolisme , Facteur de croissance fibroblastique de type 2/métabolisme , Fibroblastes/métabolisme , Flavonoïdes/pharmacologie , Système de signalisation des MAP kinases/effets des médicaments et des substances chimiques , Méthylation , Mitogen-Activated Protein Kinases/antagonistes et inhibiteurs , Myofibroblastes/anatomopathologie , Cellules NIH 3T3 , Protein Methyltransferases/métabolisme , Protein-arginine N-methyltransferases/métabolisme , Petit ARN interférent/génétique
2.
Exp. mol. med ; Exp. mol. med;: 550-560, 2011.
Article de Anglais | WPRIM | ID: wpr-131300

RÉSUMÉ

Protein arginine methylation is important for a variety of cellular processes including transcriptional regulation, mRNA splicing, DNA repair, nuclear/cytoplasmic shuttling and various signal transduction pathways. However, the role of arginine methylation in protein biosynthesis and the extracellular signals that control arginine methylation are not fully understood. Basic fibroblast growth factor (bFGF) has been identified as a potent stimulator of myofibroblast dedifferentiation into fibroblasts. We demonstrated that symmetric arginine dimethylation of eukaryotic elongation factor 2 (eEF2) is induced by bFGF without the change in the expression level of eEF2 in mouse embryo fibroblast NIH3T3 cells. The eEF2 methylation is preceded by ras-raf-mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK1/2)-p21(Cip/WAF1) activation, and suppressed by the mitogen-activated protein kinase (MAPK) inhibitor PD98059 and p21(Cip/WAF1) short interfering RNA (siRNA). We determined that protein arginine methyltransferase 7 (PRMT7) is responsible for the methylation, and that PRMT5 acts as a coordinator. Collectively, we demonstrated that eEF2, a key factor involved in protein translational elongation is symmetrically arginine-methylated in a reversible manner, being regulated by bFGF through MAPK signaling pathway.


Sujet(s)
Animaux , Souris , Arginine , Dédifférenciation cellulaire , Inhibiteur p21 de kinase cycline-dépendante/génétique , Elongation Factor 2 Kinase/métabolisme , Facteur de croissance fibroblastique de type 2/métabolisme , Fibroblastes/métabolisme , Flavonoïdes/pharmacologie , Système de signalisation des MAP kinases/effets des médicaments et des substances chimiques , Méthylation , Mitogen-Activated Protein Kinases/antagonistes et inhibiteurs , Myofibroblastes/anatomopathologie , Cellules NIH 3T3 , Protein Methyltransferases/métabolisme , Protein-arginine N-methyltransferases/métabolisme , Petit ARN interférent/génétique
3.
Article de Anglais | WPRIM | ID: wpr-211107

RÉSUMÉ

OBJECTIVE: This study was to investigate the synergistic growth inhibitory effect by combination of adenovirus mediated p53 gene transfer and cisplatin in ovarian cancer cell lines with different p53 gene mutation patterns. METHODS: Three ovarian cancer cell lines, p53 deleted SKOV3, p53 mutated OVCAR-3, and PA-1 with wild-type p53 were transduced with human adenovirus vectors carrying p53 gene (Ad-p53) and treated with a sublethal concentration of cisplatin before and after Ad-p53. The cell number was counted daily for 5 days after Ad-p53 transduction. Western blotting was used to identify p53 and p21 protein expressions, and flow cytometric analysis was performed to investigate any change of DNA ploidy after Ad-p53 transfer. RESULTS: Ad-p53 transduced cells successfully expressed p53 and p21 proteins after 48 hours of Ad-p53 transduction. Synergistic growth inhibition by combination of Ad-p53 and cisplatin was detected only in SKOV3 and OVCAR-3 cells, but not in PA-1 cells. In p53 deleted SKOV3 cells, cisplatin treatment after Ad-p53 showed higher growth inhibition than the treatment before Ad-p53 transduction, and reverse relationship was observed in p53 mutated OVCAR-3 cells. In SKOV3 cells, the fraction of cells at G2/M phase increased after cisplatin treatment, however, it decreased dramatically with Ad-p53 transduction. CONCLUSION: The synergistic growth inhibition by combination of Ad-p53 and cisplatin may depend on the p53 status and the temporal sequence of cisplatin treatment, suggesting judicious selective application of this strategy in clinical trials.


Sujet(s)
Adenoviridae , Adénovirus humains , Technique de Western , Numération cellulaire , Lignée cellulaire , Cisplatine , ADN , Gènes p53 , Thérapie génétique , Levage , Tumeurs de l'ovaire , Ploïdies , Protéines
4.
J. vet. sci ; J. vet. sci;: 105-113, 2009.
Article de Anglais | WPRIM | ID: wpr-221147

RÉSUMÉ

Inorganic phosphate (Pi) plays a critical role in diverse cellular functions, and regulating the Pi balance is accomplished by sodium-dependent Pi co-transporter (NPT). Pulmonary NPT has recently been identified in mammalian lungs. However, to date, many of the studies that have involved Pi have mainly focused on its effect on bone and kidney. Therefore, current study was performed to discover the potential effects of low Pi on the lung of developing transgenic mice expressing the renilla/firefly luciferase dual reporter gene. Two-weeks old male mice divided into 2 groups and these groups were fed either a low PI diet or a normal control diet (normal: 0.5% Pi, low: 0.1% Pi) for 4 weeks. After 4 weeks of the diet, all the mice were sacrificed. Their lungs were harvested and analyzed by performing luciferase assay, Western blotting, kinase assay and immunohistochemistry. Our results demonstrate that low Pi affects the lungs of developing mice by disturbing protein translation, the cell cycle and the expression of fibroblast growth factor-2. These results suggest that optimally regulating Pi consumption may be important to maintain health.


Sujet(s)
Animaux , Mâle , Souris , Technique de Western , Protéines de transport/métabolisme , Immunohistochimie , Poumon/effets des médicaments et des substances chimiques , Souris transgéniques , Phosphoprotéines/métabolisme , Phosphore alimentaire/administration et posologie , Phosphorylation , Phosphotransferases (Alcohol Group Acceptor)/métabolisme , Protéines proto-oncogènes c-akt/métabolisme , Cotransporteurs sodium-phosphate de type IIa/métabolisme
5.
Exp. mol. med ; Exp. mol. med;: 508-513, 2007.
Article de Anglais | WPRIM | ID: wpr-174052

RÉSUMÉ

Failure of mitotic checkpoint machinery leads to the chromosomal missegregation and nuclear endoreduplication, thereby driving the emergence of aneuploidy and tetraploidy population. Although abnormal nuclear ploidy and the resulting impairment of mitotic checkpoint function are typical physiological event leading to human hepatocellular carcinoma, any mutational change of mitotic checkpoint regulators has not yet been discovered. Therefore, we investigated the mutation of p31(comet), a recently identified mitotic checkpoint regulator, in human hepatocellular carcinoma. Of 51 human hepatocellular carcinoma tissue and 6 cell lines tested, five samples exhibited nucleotide sequence variations dispersed on four sites within the entire coding sequence. Among these sites with sequence substitutions, three were found to be missense mutation accompanied with amino acid change but one was a silent mutation. Of these sequence substitutions, two were present in both tumor and non-tumor liver tissues, suggesting the possibility of polymorphism. The present findings indicate that p31(comet) does not have an impact on the formation of aneuploidy and tetraploidy found in human hepatocellular carcinoma.


Sujet(s)
Humains , Protéines adaptatrices de la transduction du signal , Protéines de liaison au calcium/métabolisme , Carcinome hépatocellulaire/génétique , Protéines de transport/génétique , Protéines du cycle cellulaire/génétique , Lignée cellulaire tumorale , Tumeurs du foie/génétique , Mutation , Protéines nucléaires , Polyploïdie , Protéines de répression/métabolisme
6.
Exp. mol. med ; Exp. mol. med;: 491-498, 2007.
Article de Anglais | WPRIM | ID: wpr-174054

RÉSUMÉ

Axin is a negative regulator of the Wnt/beta-catenin pathway and is involved in the regulation of axis formation and proliferation. Involvement of Axin in the regulation of other signaling pathways is poorly understood. In this study, we investigated the involvement of Akt in growth regulation by Axin in L929 fibroblasts stimulated by EGF. Akt activity was increased by EGF treatment and Ras activation, respectively. Both the EGF- and Ras-induced Akt activations were abolished by Axin induction, as revealed by both Western blot and immunocytochemical analyses. The proliferation and Akt activation induced by EGF were decreased by Axin induction, and the effects of EGF were abolished by treatment of an Akt-specific inhibitor. Therefore, Axin inhibits EGF-induced proliferation of L929 fibroblasts by blocking Akt activation.


Sujet(s)
Animaux , Souris , Lignée cellulaire , Noyau de la cellule/métabolisme , Prolifération cellulaire , Facteur de croissance épidermique/pharmacologie , Fibroblastes/effets des médicaments et des substances chimiques , Protéines proto-oncogènes c-akt/antagonistes et inhibiteurs , Protéines de répression/génétique , Transduction du signal , Protéines G ras/biosynthèse
7.
Exp. mol. med ; Exp. mol. med;: 8-13, 2007.
Article de Anglais | WPRIM | ID: wpr-37560

RÉSUMÉ

Human SIRT1 controls various physiological responses including cell fate, stress, and aging, through deacetylation of its specific substrate protein. In processing DNA damage signaling, SIRT1 attenuates a cellular apoptotic response by deacetylation of p53 tumor suppressor. The present study shows that, upon exposure to radiation, SIRT1 could enhance DNA repair capacity and deacetylation of repair protein Ku70. Ectopically over-expressed SIRT1 resulted in the increase of repair of DNA strand breakages produced by radiation. On the other hand, repression of endogenous SIRT1 expression by SIRT1 siRNA led to the decrease of this repair activity, indicating that SIRT1 can regulate DNA repair capacity of cells with DNA strand breaks. In addition, we found that SIRT1 physically complexed with repair protein Ku70, leading to subsequent deacetylation. The dominant-negative SIRT1, a catalytically inactive form, did not induce deacetylation of Ku70 protein as well as increase of DNA repair capacity. These observations suggest that SIRT1 modulates DNA repair activity, which could be regulated by the acetylation status of repair protein Ku70 following DNA damage.


Sujet(s)
Humains , Sirtuines/génétique , Petit ARN interférent/génétique , Protéines de liaison à l'ADN/métabolisme , Réparation de l'ADN/génétique , ADN/génétique , Lignée cellulaire , Antigènes nucléaires/métabolisme , Acétylation
8.
J. vet. sci ; J. vet. sci;: 321-326, 2006.
Article de Anglais | WPRIM | ID: wpr-197261

RÉSUMÉ

Biocompatible silica-overcoated magnetic nanoparticles containing an organic fluorescence dye, rhodamine B isothiocyanate (RITC), within a silica shell [50 nm size, MNP@SiO2(RITC)s] were synthesized. For future application of the MNP@SiO2(RITC)s into diverse areas of research such as drug or gene delivery, bioimaging, and biosensors, detailed information of the cellular uptake process of the nanoparticles is essential. Thus, this study was performed to elucidate the precise mechanism by which the lung cancer cells uptake the magnetic nanoparticles. Lung cells were chosen for this study because inhalation is the most likely route of exposure and lung cancer cells were also found to uptake magnetic nanoparticles rapidly in preliminary experiments. The lung cells were pretreated with different metabolic inhibitors. Our results revealed that low temperature disturbed the uptake of magnetic nanoparticles into the cells. Metabolic inhibitors also prevented the delivery of the materials into cells. Use of TEM clearly demonstrated that uptake of the nanoparticles was mediated through endosomes. Taken together, our results demonstrate that magnetic nanoparticles can be internalized into the cells through an energy-dependent endosomal-lysosomal mechanism.


Sujet(s)
Humains , Matériaux biocompatibles/pharmacocinétique , Lignée cellulaire tumorale , Systèmes de délivrance de médicaments/méthodes , Endocytose/physiologie , Endosomes/physiologie , Tumeurs du poumon/traitement médicamenteux , Macrolides/pharmacologie , Microscopie confocale , Microscopie électronique à transmission , Nanoparticules/administration et posologie , Azoture de sodium/pharmacologie , Saccharose/pharmacologie , Température
9.
Yonsei med. j ; Yonsei med. j;: 811-816, 2006.
Article de Anglais | WPRIM | ID: wpr-169432

RÉSUMÉ

Expression of estrogen receptors (ER)-alpha and -beta, as well as androgen receptor (AR), in hepatocellular carcinoma (HCC) is thought to be correlated with prognosis, survival, and male prevalence of HCC. These hypotheses are based on investigations of European patients; however the expression patterns of these receptors in Asian patients are largely unknown. In this study, we collected liver carcinoma and peritumor tissues from 32 patients (9 females and 23 males) in South Korea. The expression of ERs and ARs was studied using RT-PCR. Wild-type ER-alpha and AR were expressed in all of the samples investigated, and their expression was independent of the causal virus or patient sex. Expression of the ER-alpha variant was independent of sex (100% female vs. 91.3% male) and HCV and HBV status (91.3% vs. 100%). Wild-type ER-beta was expressed more often in HCV patients than in HBV patients (95.7% vs. 44.4%; p < 0.05). In conclusion, the stronger ER-alpha variant expression in HCC tissues implies that this variant has an important role in HCC development. However, at least in Korean patients, expression of the ER-alpha variant (vER-alpha) is not related to male HCC prevalence. In addition, the predominant expression of ER-beta in HCV patients suggests that it plays an important role in HCV-induced liver disease.


Sujet(s)
Adulte d'âge moyen , Mâle , Humains , Femelle , Sujet âgé , Facteurs sexuels , Récepteurs des oestrogènes/métabolisme , Récepteurs aux androgènes/métabolisme , Tumeurs du foie/ethnologie , Corée , Virus de l'hépatite B/isolement et purification , Hepacivirus/isolement et purification , Carcinome hépatocellulaire/ethnologie , Marqueurs biologiques/métabolisme , Asiatiques
10.
Article de Anglais | WPRIM | ID: wpr-98120

RÉSUMÉ

Ras-related, estrogen-regulated, and growth-inhibitory gene (RERG) is a novel gene that was first reported in breast cancer. However, the functions of RERG are largely unknown in other tumor types. In this study, RERG expression was analyzed in hepatocellular carcinomas of human patients using reverse transcriptase PCR analysis. In addition, the possible regulation of RERG expression by histone deacetyltransferases (HDACs) was studied in several cell lines. Interestingly, the expression of RERG gene was increased in hepatocellular carcinoma (HCC) of male patients (57.9%) but decreased in HCC of females (87.5%) comparison with paired peri-tumoral tissues. Moreover, RERG gene expression was increased in murine hepatoma Hepa1-6 cells, human breast tumor MDA-MB-231 cells, and mouse normal fibroblast NIH3T3 cells after treated by HDAC inhibitor, trichostatin A. Our results suggest that RERG may function in a gender-dependent manner in hepatic tumorigenesis and that the expression of this gene may be regulated by an HDAC-related signaling pathway.


Sujet(s)
Souris , Mâle , Humains , Femelle , Animaux , Transduction du signal , Facteurs sexuels , Souris transgéniques , Souris de lignée C57BL , Tumeurs du foie/génétique , Histone deacetylases/physiologie , Hépatocytes/métabolisme , Inhibiteurs de croissance/génétique , Gènes ras , Régulation de l'expression des gènes tumoraux , Oestrogènes/pharmacologie , Récepteur alpha des oestrogènes/analyse , Prolifération cellulaire
11.
Exp. mol. med ; Exp. mol. med;: 686-693, 2006.
Article de Anglais | WPRIM | ID: wpr-106416

RÉSUMÉ

The gradual loss of telomeric DNA can contribute to replicative senescence and thus, having longer telomeric DNA is generally considered to provide a longer lifespan. Maintenance and stabilization of telomeric DNA is assisted by binding of multiple DNA-binding proteins, including those involved in double strand break (DSB) repair. We reasoned that declining DSB repair capacity and increased telomere shortening in aged individuals may be associated with decreased expression of DSB repair proteins capable of telomere binding. Our data presented here show that among the DSB repair proteins tested, only the expression of Ku70 and Mre11 showed statistically significant age-dependent changes in human lymphocytes. Furthermore, we found that expressions of Ku70 and Mre11 are statistically correlated, which indicate that the function of Ku70 and Mre11 may be related. All the other DSB repair proteins tested, Sir2, TRF1 and Ku80, did not show any significant differences upon aging. In line with these data, people who live in the regional community (longevity group), which was found to have statistically longer average life span than the rest area, shows higher level of Ku70 expression than those living in the neighboring control community. Taken together, our data show, for the first time, that Ku70 and Mre11 may represent new biomarkers for aging and further suggest that maintenance of higher expression of Ku70 and Mre11 may be responsible for keeping longer life span observed in the longevity group.


Sujet(s)
Adulte d'âge moyen , Humains , Sujet âgé de 80 ans ou plus , Sujet âgé , Adulte , Télomère/génétique , Longévité , Protéines de liaison à l'ADN/métabolisme , Réparation de l'ADN/génétique , ADN/génétique , Vieillissement de la cellule/physiologie , Lymphocytes T CD4+/métabolisme , Antigènes nucléaires/métabolisme , Vieillissement/physiologie
12.
Exp. mol. med ; Exp. mol. med;: 255-260, 2005.
Article de Anglais | WPRIM | ID: wpr-201935

RÉSUMÉ

Sec13p has been known as an endoplasmic reticulum-Golgi transport protein. Recently, it has also been shown to be required for the formation of septation in the fission yeast Schizosaccharomyces pombe. In the present study, we focused on the role of a human homolog of Saccharomyces cerevisiae SEC13, Sec13 protein during mitosis in U2OS cells. We found that the expression of Sec13 was constant throughout the cell cycle, and localized to the kinetochores at metaphase during mitosis. By using green fluorescent protein technology, we observed that Sec13 is required for evasion of mitotic arrest in response to spindle damage, leading to G1-like phase and apoptotic cell death. In addition, cells expressing exogenous Sec13 showed giant nuclei compared to endogenous ones in the absence of nocodazole. These results demonstrate that Sec13 is involved in the regulation of the metaphase/anaphase transition and may be functionally associated with mitotic machinery to maintain genomic stability during mitosis.


Sujet(s)
Humains , Anaphase , Antinéoplasiques/pharmacologie , Lignée cellulaire tumorale/effets des médicaments et des substances chimiques , Phase G1 , Instabilité du génome , Protéines à fluorescence verte/métabolisme , Kinétochores/métabolisme , Protéines membranaires/génétique , Métaphase , Mitose/physiologie , Appareil du fuseau , Nocodazole/pharmacologie , Ostéosarcome/génétique
13.
Article de Coréen | WPRIM | ID: wpr-94682

RÉSUMÉ

BACKGROUND/AIMS: The prevalence of hepatitis delta virus (HDV) infection has been estimated as being approximately 5% among global HBsAg carriers. The anti-delta positive rate in Koreans had been reported as being 0.85% in 1985. While the prevalence of HBV has been decreased from nearly 10% to 5% during the past twenty years, there have been no more studies on the anti-delta prevalence in Koreans. The aim of this study was to estimate the anti-delta prevalence in Koreans and to study the clinical characteristics of anti-delta positive patients in a single center. METHODS: Serum anti-delta was measured in one hundred ninety four HBsAg-positive patients who were admitted to our hospital from February 2003 to August 2003. We checked the genotypes of the HBV in the anti-delta positive patients. The clinical features of the anti-delta positive patients were compared to those clinical features of the anti-delta negative patients from the aspect of age, gender, mode of transmission, the positivity of HBeAg and serum HBV DNA. RESULTS: Serum anti-delta was positive in seven patients among the 194 subjects, giving a 3.6% positive rate. Among these seven patients, six had hepatocellular carcinoma (HCC) and the other one had cholangiocarcinoma. All of the anti-delta positive patients had the C genotype of HBV. The anti-delta positive patients showed significantly suppressed HBV DNA replication compared to the anti-delta negative patients. CONCLUSIONS: In Koreans, anti-delta was positive mainly in HCC patients with an approximate prevalence of 4%, and this rate has not changed much for the past twenty years. HBV DNA replication was suppressed by HDV infection.


Sujet(s)
Adulte , Femelle , Humains , Mâle , Adulte d'âge moyen , Carcinome hépatocellulaire/virologie , Résumé en anglais , Anticorps de l'hépatite/analyse , Hépatite D/complications , Virus de l'hépatite delta/immunologie , Antigènes de l'hépatite virale delta/analyse , Corée/épidémiologie , Tumeurs du foie/virologie , Prévalence
14.
J. vet. sci ; J. vet. sci;: 369-378, 2004.
Article de Anglais | WPRIM | ID: wpr-79776

RÉSUMÉ

Evidences show that eukaryotic mRNAs can perform protein translation through internal ribosome entry sites (IRES). 5'-Untranslated region of the mRNA encoding apoptotic protease-activating factor 1 (Apaf-1) contains IRES, and, thus, can be translated in a cap-independent manner. Effects of changes in protein translation pattern through rapamycin pretreatment on 4-(methylnitrosamino)-1-(3-pyridyl)-butanone(NNK, tobacco-specific lung carcinogen)-induced apoptosis in human bronchial epithelial cells were examined by caspase assay, FACS analysis, Western blotting, and transient transfection. Results showed that NNK induced apoptosis in concentration- and time-dependent manners. NNK-induced apoptosis occurred initially through cap-independent protein translation, which during later stage was replaced by cap-dependent protein translation. Our data may be pplicable as the mechanical basis of lung cancer treatment.


Sujet(s)
Humains , Antibiotiques antinéoplasiques/pharmacologie , Apoptose/effets des médicaments et des substances chimiques , Facteur-1 activateur des protéases apoptotiques , Protéine Bid , Technique de Western , Bronches/métabolisme , Cancérogènes/pharmacologie , Protéines de transport/métabolisme , Caspases/métabolisme , Cytochromes c/métabolisme , Relation dose-effet des médicaments , Cellules épithéliales/métabolisme , Facteur-4E d'initiation eucaryote/métabolisme , Cytométrie en flux , Nitrosamines/pharmacologie , Biosynthèse des protéines , Protéines/métabolisme , Protéines proto-oncogènes c-bcl-2/métabolisme , Protéines de liaison à la coiffe de l'ARN/physiologie , Sirolimus/pharmacologie , Facteurs temps , Protéine Bax
15.
Article de Coréen | WPRIM | ID: wpr-194500

RÉSUMÉ

BACKGROUND/AIMS: The aims of our study are to assess the frequency of peripheral blood mononuclear cell (PBMC) proliferation and cytokine profiles to hepatitis C virus (HCV) core protein and NS3 protein to search the potential immunosuppressive effect of HCV core in chronically HCV-infected patients. Subjects and METHODS: Thirty two anti-HCV-positive patients with chronic liver diseases, eight HBsAg-positive patients with chronic liver diseases, and six healthy adults were the subjects of our study. Using recombinant HCV core and NS3, proliferative response of PBMC and cytokine production were determined. RESULTS: Fifty nine percent and thirteen percent of patients with HCV-related chronic liver diseases showed positive PBMC proliferation to HCV core and NS3, respectively. Thirty four percent and fifty nine percent of patients with HCV-related chronic liver diseases showed significant production of interferon-gamma to HCV core and NS3, respectively. IL-4 production was negligible. When the PBMC were treated with HCV core and NS3 concurrently, or HCV core and phytohemagglutinin concurrently, the stimulation indices were significantly decreased compared to those treated either with NS3 or PHA without core. CONCLUSIONS: Although about two thirds of chronically HCV-infected patients with liver diseases showed the PBMC proliferation and Th 1 type cytokine profile, they could not eradicate the viral infection. This ineffective immune response seems to play a role in the pathogenesis of chronic inflammatory liver disease resulting in liver cirrhosis and hepatocellular carcinoma. HCV core showed a potential immunosuppressive effect, which has important meaning for the mechanism of HCV persistence.


Sujet(s)
Adulte , Humains , Carcinome hépatocellulaire , Hepacivirus , Hépatite C chronique , Hépatite chronique , Immunosuppression thérapeutique , Interféron gamma , Interleukine-4 , Cirrhose du foie , Maladies du foie
16.
Korean Circulation Journal ; : 369-380, 1990.
Article de Coréen | WPRIM | ID: wpr-35176

RÉSUMÉ

In order to observe the development of arrhythmia during regional myocardial ischemia and reperfusion. Proximal left descending coronary artery(LAD) was ligated for 20 minutes and reperfused suddenly in fifty one cats which were grouped into control(n=16), alpha-receptor block group(n=8), beta-receptor block group (n=9), parasymphathetic system block group (n=10) and autonomic nervous system block group(n=8). In drug infused groups, drug infusion was started 5 minutes prior to occlusion with bolus. Epicardial electrocardiogram, left ventricular pressure and standard ECG(lead I) were simultaneously recorded with the paper speed of 25mm/sec at predetermined time intervals and when arrhythmias occurred, and those were recorded continuousely with the paper speed of 5mm/sec throughout the experiment. The results were as follows : 1) After ligation of LAD, the R wave and ST segment of QRS of epicardial ECG elevated to reach maximum level with first 10 minutes. 2) The incidence of occlusion ventricular tachycardia in autonomic nervous system block group and alpha-receptor block group was significantly lower than control group(P<0.01). 3) The incidence of reperfusion ventricular tachycardial and ventricular fibrillation in autonomic nervous system block group, beta-receptor block group and alpha-receptor block group was significantly lower than control group(P<0.05). 4) The arrhythmia score during LAD occlusion in autonomic nervous system block group and alpha-receptor block group was significantly lower than control group(P<0.05). 5) The arrhythmia score in reperfusion in autonomic nervous system block group, beta-receptor block group and alpha-receptor block group was significantly lower than control group (P<0.05). It was concluded that the reperfusion arrhythmia could be prevented by alpha-receptor and beta-receptor block. There was the synergism between alpha-receptor blocker and beta-receptor blokcer. But the occlusion arrhythmia was suppressed by only alpha-receptor blocker.


Sujet(s)
Animaux , Chats , Troubles du rythme cardiaque , Système nerveux autonome , Électrocardiographie , Incidence , Ligature , Ischémie myocardique , Reperfusion , Tachycardie ventriculaire , Fibrillation ventriculaire , Pression ventriculaire
17.
Yonsei med. j ; Yonsei med. j;: 255-260, 1987.
Article de Anglais | WPRIM | ID: wpr-52780

RÉSUMÉ

The activities of Ca+2-PL dependent protein Kinase (PKC) and independent protein kinase(RKM) were measured in human stomach and breast tumors and in the respective counterparts of normal tissue. Expression of c-fos and c-myc of the tissues were also measured. RNAs of c-fos and c-myc were unexpectedly high in the tissue from normal stomach and breast as well as in all cancer tissue. On the other hand, cytosolic and particulate PKC activities were higher in the tumors as compared to those of normal controls. Notably, some cases exhibited. altered activities of PKC i.e. increased RKM activities as high as RKC, which might be related to the autocrine control of growth in the tumor mass.


Sujet(s)
Humains , Adénocarcinome/enzymologie , Tumeurs du sein/enzymologie , Carcinome intracanalaire non infiltrant/enzymologie , Protéine kinase C/métabolisme , Tumeurs de l'estomac/enzymologie
18.
Yonsei med. j ; Yonsei med. j;: 38-48, 1987.
Article de Anglais | WPRIM | ID: wpr-26449

RÉSUMÉ

We investigated the pathobiological course of uranyl nitrate (UN) induced polyuric acute tubular necrosis (ATN) in male Sprague Dawley rats. UN (5mg/kg 15mg/kg and 3Omg/kg) in 5% NaHCO3 induced weight loss, polydipsia, and polyuria 24 hrs after injection when compared to the controls which were treated with 5% NaHCO3 only. Twenty four hours following the injection of UN, serum creatinine and blood urea nitrogen levels had increased. These changes continued for at least 72 hours, although the concentration of uranium had decreased. Light microscopic studies conducted 24 hours after injection, revealed partial degeneration and necrosis of the proximal tubules and many casts m the distal convoluted tubules. These changes progressed for 72 hours. Despite this tubular damage, the glomeruli were relatively intact. 5 days after injection, the epithelial cells lining the proximal tubules displayed regenerative activities; these findings were more prominent after 10 days. Through electron microscopic examination, we observed the destruction of mitochondria in the proximal tubular cells, a possible cause of polyuria. Ten days post injection regenerative activities in the proximal tubular cells showed that the maturation of intracellular organelles followed the proliferation of the premature cells.


Sujet(s)
Mâle , Rats , Animaux , Atteinte rénale aigüe/induit chimiquement , Tests de la fonction rénale , Néphropathie tubulo-interstitielle aigüe/induit chimiquement , Lignées consanguines de rats , Uranium/pharmacologie , Nitrate d'uranyle/pharmacologie
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