1.Effects of Mycobacterium leprae , M . leprae Phenolic Glycolipid - 1 and Cytokines on the Nitric Oxide Generation of RAW 264 . 7 Macrophages.
Seok Don PARK ; Jae Sung LEE ; Bok Soo LEE ; Chang Duk JUN ; Hun Taeg CHUNG ; Jong Gu KIM
Korean Journal of Dermatology 1994;32(2):234-244
Background: Nitric oxide(NO) has been reproted to play an important role in macrophage-mediated microbicidal capacity for a variety of intracellular pathogens. NO generation is used as an indicator of microbicidal function of macrophages. OBJECTIVE: Our purpose is to investigate the production of NO rom macrophages phagocytized with Mycobacterium leprae or M. leprae phenolic glycolipid-1(PGL-1) for the purpose of elucidating the pathogenesis of leprosy. METHODS: We used a murine macrophage cell line, RAW 264.7. Macrophages were incubated with dead M. leprae or PGL-1, respectively and then treated with interfer n-gamma(IFN-r) and/or tumor necrosis factor-alpha(TNF-a). The release of NO was determined spectrophotometrically by measuring nitrite. RESULTS: M. Leprae and PGL-1 failed to stimulnte NO secretion execept at high bacteria-to-cell rations(50:1)and at the higheat concentrat,ion(100pg/ml) of PGL-1. IFN-r or IFN-r plus TNF-a markedly stimulated macrophages phagocyt,ized with M. leprae or PGL-1 to release NO . CONCLUSION: Defective IFN-r-dependent NO production of macrophages may be an important factor in the pathogenesis of leprosy.
Cell Line
;
Cytokines*
;
Leprosy
;
Macrophages*
;
Mycobacterium leprae*
;
Mycobacterium*
;
Necrosis
;
Nitric Oxide*
;
Phenol*
2.The Study about Expression and Regulation Mechanism of Heat Shock Protein 70 by Arisostatins A in Caki Cell Line of Renal Cell Carcinoma.
Hwa LEE ; Taeg Kyu KWON ; Jong Wook PARK ; Kyung Seop LEE
Korean Journal of Urology 2005;46(2):181-189
PURPOSE: The events of cell stress and cell death are linked, with the heat shock proteins (Hsps) induced in response to stress appearing to function at key regulatory points in the control of apoptosis. The purpose of this study was to investigate the effect of arisostatins A on the Hsp70 expression and signal mechanism of its transcription. MATERIALS AND METHODS: We used natural arisostatins A produced by Actinomycete, in Caki cells. We measured the growth rate of cell using trypan blue staining, and the induction of the transcriptional levels of Hsp70 with arisostatins, which was quantified by reverse transcript-polymerase chain reaction (RT-PCR) and transiently transfecting cells with a Hsp70. The induction of the transcriptional levels of Hsp70 with arisostatins A was quantified by RT-PCR and transiently transfecting cells with a Hsp70 promoter-luciferase reporter plasmid. RESULTS: Arisostatins A-induced Hsp70 up-regulation was not prevented by the overexpression of peroxiredoxinI (PrxI), PrxII or treatment of superoxide dismutase and catalase. However, the arisostatins A-mediated expression of Hsp70 was reduced significantly in Caki cells treated by the antioxidant, N-acetylcystein. Inhibition of the Janus tyrosine kinase (JAK) activity with AG490 did not inhibit the arisostatins A-induced Hsp70 up-regulation, suggesting that JAK is not associated with the arisostatins A-mediated Hsp70 expression. The mechanism of Hsp70 induction depends on the activation of heat shock factor-1. However, arisostatins A did not effect the change in the expression levels of heat shock factor-1. CONCLUSIONS: These findings suggested that Hsp directly regulates specific stress-responsive signaling pathways, which may antagonize the signaling cascades that result in apoptosis.
Apoptosis
;
Carcinoma, Renal Cell*
;
Catalase
;
Cell Death
;
Cell Line*
;
Heat-Shock Proteins*
;
Hot Temperature*
;
HSP70 Heat-Shock Proteins*
;
Plasmids
;
Protein-Tyrosine Kinases
;
Shock
;
Superoxide Dismutase
;
Trypan Blue
;
Up-Regulation
3.Development of Personalized Urination Recognition Technology Using Smart Bands.
Sung Jong EUN ; Taeg Keun WHANGBO ; Dong Kyun PARK ; Khae Hawn KIM
International Neurourology Journal 2017;21(Suppl 1):S76-S83
PURPOSE: This study collected and analyzed activity data sensed through smart bands worn by patients in order to resolve the clinical issues posed by using voiding charts. By developing a smart band-based algorithm for recognizing urination activity in patients, this study aimed to explore the feasibility of urination monitoring systems. METHODS: This study aimed to develop an algorithm that recognizes urination based on a patient's posture and changes in posture. Motion data was obtained from a smart band on the arm. An algorithm that recognizes the 3 stages of urination (forward movement, urination, backward movement) was developed based on data collected from a 3-axis accelerometer and from tilt angle data. Real-time data were acquired from the smart band, and for data corresponding to a certain duration, the absolute value of the signals was calculated and then compared with the set threshold value to determine the occurrence of vibration signals. In feature extraction, the most essential information describing each pattern was identified after analyzing the characteristics of the data. The results of the feature extraction process were sorted using a classifier to detect urination. RESULTS: An experiment was carried out to assess the performance of the recognition technology proposed in this study. The final accuracy of the algorithm was calculated based on clinical guidelines for urologists. The experiment showed a high average accuracy of 90.4%, proving the robustness of the proposed algorithm. CONCLUSIONS: The proposed urination recognition technology draws on acceleration data and tilt angle data collected via a smart band; these data were then analyzed using a classifier after comparative analyses with standardized feature patterns.
Acceleration
;
Arm
;
Humans
;
Posture
;
Urination*
;
Vibration
4.In Silico Analysis for Sphingolipid Metabolism-Related Genes in Human Kidney Clear Cell Carcinoma Using The Cancer Genome Atlas.
Woo-Jae PARK ; Jee Young PARK ; Taeg Kyu KWO ; Jong-Wook PARK ; Shin KIM
Keimyung Medical Journal 2020;39(1):14-22
The sphingolipid rheostat concept states that the cellular fate is largely determined by various sphingolipid metabolites and the associated signaling pathways. Aberrant regulation of the sphingolipid metabolism-related components is closely associated with cancer survival and death, including aspects like cancer development, proliferation, progression, and response to anticancer drugs. In the present study, we investigated the expression and prognostic significance of the sphingolipid metabolism-related genes in clear cell renal cell carcinoma (ccRCC), the most common pathological subtype of kidney cancer, using an RNA-sequencing dataset of The Cancer Genome Atlas Kidney Clear Cell Carcinoma (TCGA KIRC) cohort. Expression levels of various sphingolipid metabolism-related genes were significantly altered in ccRCC tissues compared with those of normal solid tissues. Notably, the expression of B4GALNT1, BNIP3, DEGS1, GAL3ST1, S1PR4, SLC26A10, SMPDL3A, and SPHK1 was significantly upregulated, whereas the expression of B4GALT6, HPGD, LPAR1, SFTPB, ST6GALNAC5, and UGT8 was significantly downregulated in ccRCC tissues. Notably, among these significantly-altered sphingolipid metabolism-related genes, the Kaplan-Meier survival analyses showed that high expression levels of B4GALNT1, SLC26A10, and SPHK1 were associated with a poor prognosis of patients with ccRCC, whereas high expression levels of BNIP3, HPGD, and SMPDL3A were associated with a better prognosis. Taken together, our study suggests that B4GALNT1, SLC26A10, SPHK1, BNIP3, HPGD, and SMPDL3A may be novel prognostic biomarkers and targets for a therapeutic strategy to improve the treatment of ccRCC.
5.Effect of Combined Treatment of Metoclopramide With Platinum-Based Drugs on Apoptosis in AMC-HN4 Cells
Jong Won PARK ; Seon Min WOO ; Jong In JEONG ; Jae Man LEE ; Ji Won LEE ; Dong Eun KIM ; Taeg Kyu KWON
Korean Journal of Otolaryngology - Head and Neck Surgery 2025;68(3):113-120
Background and Objectives:
Metoclopramide is an antagonist of dopamine D2 receptor and is capable of alleviating chemotherapy-induced nausea and vomiting. However, its underlying mechanisms and function in improving the efficiency of chemotherapy are not fully understood. In this study, we investigated the sensitizing effect of metoclopramide on the platinum-based drugs-mediated apoptosis in human head and neck cancer cells.Subjects and Method Apoptosis was analyzed using a cell-based cytometer. The protein expression and messenger ribonucleic acid (mRNA) levels were assessed by Western blotting and real-time polymerase chain reaction, respectively.
Results:
Metoclopramide sensitized the platinum-based drug (cisplatin and oxaliplatin)-mediated apoptosis in AMC-HN4 cells, but not in normal cells. Mechanistically, we found that metoclopramide decreased Mcl-1 protein expression through post-translational regulation. Moreover, the overexpression of Mcl-1 prevented apoptosis by combined treatment of metoclopramide and platinum-based drugs.
Conclusion
Metoclopramide induced proteasome-mediated Mcl-1 downregulation, resulting in increased sensitivity to platinum-based drugs.
6.Effect of Combined Treatment of Metoclopramide With Platinum-Based Drugs on Apoptosis in AMC-HN4 Cells
Jong Won PARK ; Seon Min WOO ; Jong In JEONG ; Jae Man LEE ; Ji Won LEE ; Dong Eun KIM ; Taeg Kyu KWON
Korean Journal of Otolaryngology - Head and Neck Surgery 2025;68(3):113-120
Background and Objectives:
Metoclopramide is an antagonist of dopamine D2 receptor and is capable of alleviating chemotherapy-induced nausea and vomiting. However, its underlying mechanisms and function in improving the efficiency of chemotherapy are not fully understood. In this study, we investigated the sensitizing effect of metoclopramide on the platinum-based drugs-mediated apoptosis in human head and neck cancer cells.Subjects and Method Apoptosis was analyzed using a cell-based cytometer. The protein expression and messenger ribonucleic acid (mRNA) levels were assessed by Western blotting and real-time polymerase chain reaction, respectively.
Results:
Metoclopramide sensitized the platinum-based drug (cisplatin and oxaliplatin)-mediated apoptosis in AMC-HN4 cells, but not in normal cells. Mechanistically, we found that metoclopramide decreased Mcl-1 protein expression through post-translational regulation. Moreover, the overexpression of Mcl-1 prevented apoptosis by combined treatment of metoclopramide and platinum-based drugs.
Conclusion
Metoclopramide induced proteasome-mediated Mcl-1 downregulation, resulting in increased sensitivity to platinum-based drugs.
7.Effect of Combined Treatment of Metoclopramide With Platinum-Based Drugs on Apoptosis in AMC-HN4 Cells
Jong Won PARK ; Seon Min WOO ; Jong In JEONG ; Jae Man LEE ; Ji Won LEE ; Dong Eun KIM ; Taeg Kyu KWON
Korean Journal of Otolaryngology - Head and Neck Surgery 2025;68(3):113-120
Background and Objectives:
Metoclopramide is an antagonist of dopamine D2 receptor and is capable of alleviating chemotherapy-induced nausea and vomiting. However, its underlying mechanisms and function in improving the efficiency of chemotherapy are not fully understood. In this study, we investigated the sensitizing effect of metoclopramide on the platinum-based drugs-mediated apoptosis in human head and neck cancer cells.Subjects and Method Apoptosis was analyzed using a cell-based cytometer. The protein expression and messenger ribonucleic acid (mRNA) levels were assessed by Western blotting and real-time polymerase chain reaction, respectively.
Results:
Metoclopramide sensitized the platinum-based drug (cisplatin and oxaliplatin)-mediated apoptosis in AMC-HN4 cells, but not in normal cells. Mechanistically, we found that metoclopramide decreased Mcl-1 protein expression through post-translational regulation. Moreover, the overexpression of Mcl-1 prevented apoptosis by combined treatment of metoclopramide and platinum-based drugs.
Conclusion
Metoclopramide induced proteasome-mediated Mcl-1 downregulation, resulting in increased sensitivity to platinum-based drugs.
8.Effect of Combined Treatment of Metoclopramide With Platinum-Based Drugs on Apoptosis in AMC-HN4 Cells
Jong Won PARK ; Seon Min WOO ; Jong In JEONG ; Jae Man LEE ; Ji Won LEE ; Dong Eun KIM ; Taeg Kyu KWON
Korean Journal of Otolaryngology - Head and Neck Surgery 2025;68(3):113-120
Background and Objectives:
Metoclopramide is an antagonist of dopamine D2 receptor and is capable of alleviating chemotherapy-induced nausea and vomiting. However, its underlying mechanisms and function in improving the efficiency of chemotherapy are not fully understood. In this study, we investigated the sensitizing effect of metoclopramide on the platinum-based drugs-mediated apoptosis in human head and neck cancer cells.Subjects and Method Apoptosis was analyzed using a cell-based cytometer. The protein expression and messenger ribonucleic acid (mRNA) levels were assessed by Western blotting and real-time polymerase chain reaction, respectively.
Results:
Metoclopramide sensitized the platinum-based drug (cisplatin and oxaliplatin)-mediated apoptosis in AMC-HN4 cells, but not in normal cells. Mechanistically, we found that metoclopramide decreased Mcl-1 protein expression through post-translational regulation. Moreover, the overexpression of Mcl-1 prevented apoptosis by combined treatment of metoclopramide and platinum-based drugs.
Conclusion
Metoclopramide induced proteasome-mediated Mcl-1 downregulation, resulting in increased sensitivity to platinum-based drugs.
9.Effect of Combined Treatment of Metoclopramide With Platinum-Based Drugs on Apoptosis in AMC-HN4 Cells
Jong Won PARK ; Seon Min WOO ; Jong In JEONG ; Jae Man LEE ; Ji Won LEE ; Dong Eun KIM ; Taeg Kyu KWON
Korean Journal of Otolaryngology - Head and Neck Surgery 2025;68(3):113-120
Background and Objectives:
Metoclopramide is an antagonist of dopamine D2 receptor and is capable of alleviating chemotherapy-induced nausea and vomiting. However, its underlying mechanisms and function in improving the efficiency of chemotherapy are not fully understood. In this study, we investigated the sensitizing effect of metoclopramide on the platinum-based drugs-mediated apoptosis in human head and neck cancer cells.Subjects and Method Apoptosis was analyzed using a cell-based cytometer. The protein expression and messenger ribonucleic acid (mRNA) levels were assessed by Western blotting and real-time polymerase chain reaction, respectively.
Results:
Metoclopramide sensitized the platinum-based drug (cisplatin and oxaliplatin)-mediated apoptosis in AMC-HN4 cells, but not in normal cells. Mechanistically, we found that metoclopramide decreased Mcl-1 protein expression through post-translational regulation. Moreover, the overexpression of Mcl-1 prevented apoptosis by combined treatment of metoclopramide and platinum-based drugs.
Conclusion
Metoclopramide induced proteasome-mediated Mcl-1 downregulation, resulting in increased sensitivity to platinum-based drugs.
10.A Combination of PG490 and Lipopolysaccharide Induce Apoptosis through Activation of Casapase-3 and Down- regulation of cIAP1 and XIAP in Human Astroglioma Cell.
Tae Jin LEE ; Kyung Jin WOO ; Jong Wook PARK ; Taeg Kyu KWON
Immune Network 2005;5(2):99-104
BACKGROUND: Malignant gliomas are the most common primary tumors in the central nervous system. METHODS: We investigated the combined effect of PG490 and LPS on the induction of the apoptotic pathway in human astroglioma cells. RESULTS: Treatment of U87 cells with combination of 50 nM of PG490 and 50microgram/ml of LPS resulted in increased internucleosomal DNA fragmentation, cleavage of PLC-gamma1, and down- regulation of cIAP1 and XIAP. The combination of LPS and PG490 treatment-induced apoptosis is mediated through the activation of caspase, which is inhibited by the caspase inhibitor, z-VAD-fmk. Also, release of cytochrome c was found in PG490 and LPS- cotreated U87 cell. CONCLUSION: Taken together, combination of PG490 and LPS appears to be a potent inducer of apoptosis in astrogliaoma cells, and might have some benefit in the treatment of glioma patients.
Apoptosis*
;
Astrocytoma*
;
Central Nervous System
;
Cytochromes c
;
DNA Fragmentation
;
Glioma
;
Humans*