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      • Spontaneous high-frequency action potential.

        Shen, Haiying,Choe, Wonchae Jointly published by Science China Press and Sprin 2011 Science China. Life sciences Vol.54 No.4

        <P>Action potential, which is the foundation of physiology and electrophysiology, is most vital in physiological research. This work starts by detecting cardiac electrophysiology (tachyarrhythmias), combined with all spontaneous discharge phenomena in vivo such as wound currents and spontaneous neuropathic pain, elaborates from generation, induction, initiation, to all of the features of spontaneous high-frequency action potential-SSL action potential mechanism, i.e., connecting-end hyperpolarization initiates spontaneous depolarization and action potential in somatic membrane. This work resolves the conundrums of in vivo spontaneous discharge in tachyarrhythmias, wounds, denervation supersensitivity, neurogenic pain (hyperalgesia and allodynia), epileptic discharge and diabetic pain in pathophysiological and clinical researches that have puzzled people for a hundred years.</P>

      • KCI등재

        AMP-activated protein kinase determines apoptotic sensitivity of cancer cells to ginsenoside-Rh2

        Min-Jung Kim,Hee Yun,Dong-Hyun Kim,Insug Kang,Wonchae Choe,Sung-Soo Kim,Joohun Ha 고려인삼학회 2014 Journal of Ginseng Research Vol.38 No.1

        Ginseng saponins exert various important pharmacological effects with regard to the control of many diseases, including cancer. In this study, the anticancer effect of ginsenosides on human cancer cells was investigated and compared. Among the tested compounds, ginsenoside-Rh2 displays the highest inhibitory effect on cell viability in HepG2 cells. Ginsenoside-Rh2, a ginseng saponin isolated from the root of Panax ginseng, has been suggested to have potential as an anticancer agent, but the underlying mechanisms remain elusive. In the present study, we have shown that cancer cells have differential sensitivity to ginsenoside-Rh2-induced apoptosis, raising questions regarding the specific mechanisms responsible for the discrepant sensitivity to ginsenoside-Rh2. In this study, we demonstrate that AMPactivated protein kinase (AMPK) is a survival factor under ginsenoside-Rh2 treatment in cancer cells. Cancer cells with acute responsiveness of AMPK display a relative resistance to ginsenoside-Rh2, but cotreatment with AMPK inhibitor resulted in a marked increase of ginsenoside-Rh2-induced apoptosis. We also observed that p38 MAPK (mitogen-activated protein kinase) acts as another survival factor under ginsenoside-Rh2 treatment, but there was no signaling crosstalk between AMPK and p38 MAPK, suggesting that combination with inhibitor of AMPK or p38 MAPK can augment the anticancer potential of ginsenoside Rh2.

      • SCIESCOPUSKCI등재

        AMP-activated protein kinase determines apoptotic sensitivity of cancer cells to ginsenoside-Rh2

        Kim, Min-Jung,Yun, Hee,Kim, Dong-Hyun,Kang, Insug,Choe, Wonchae,Kim, Sung-Soo,Ha, Joohun The Korean Society of Ginseng 2014 Journal of Ginseng Research Vol.38 No.1

        Ginseng saponins exert various important pharmacological effects with regard to the control of many diseases, including cancer. In this study, the anticancer effect of ginsenosides on human cancer cells was investigated and compared. Among the tested compounds, ginsenoside-Rh2 displays the highest inhibitory effect on cell viability in HepG2 cells. Ginsenoside-Rh2, a ginseng saponin isolated from the root of Panax ginseng, has been suggested to have potential as an anticancer agent, but the underlying mechanisms remain elusive. In the present study, we have shown that cancer cells have differential sensitivity to ginsenoside-Rh2-induced apoptosis, raising questions regarding the specific mechanisms responsible for the discrepant sensitivity to ginsenoside-Rh2. In this study, we demonstrate that AMP-activated protein kinase (AMPK) is a survival factor under ginsenoside-Rh2 treatment in cancer cells. Cancer cells with acute responsiveness of AMPK display a relative resistance to ginsenoside-Rh2, but cotreatment with AMPK inhibitor resulted in a marked increase of ginsenoside-Rh2-induced apoptosis. We also observed that p38 MAPK (mitogen-activated protein kinase) acts as another survival factor under ginsenoside-Rh2 treatment, but there was no signaling crosstalk between AMPK and p38 MAPK, suggesting that combination with inhibitor of AMPK or p38 MAPK can augment the anticancer potential of ginsenoside Rh2.

      • Antioxidant activity is required for the protective effects of cyclophilin A against oxidative stress

        KIM, KIYOON,OH, IN KYUNG,YOON, KYUNG SIK,HA, JOOHUN,KANG, INSUG,CHOE, WONCHAE SPANDIDOS PUBLICATIONS 2015 MOLECULAR MEDICINE REPORTS Vol.12 No.1

        <P>Cyclophilin (Cyp) belongs to a group of proteins that have peptidyl-prolyl cis-trans isomerase (PPIase) activity. CypA is the major cellular target for the immunosuppressive drug cyclosporin A and mediates its actions. Previous studies have demonstrated that CypA has diverse cellular functions and have suggested that CypA may function as an antioxidant. The present study investigated the antioxidant activity of CypA and its association with PPIase activity. The purified CypA/wild-type (WT) and CypA/P16S mutant proteins were active in PPIase assays. A total antioxidant capacity assay revealed that the purified CypA/WT protein had significantly higher antioxidant activity, whereas the CypA/P16S mutant was defective in its antioxidant activity. To confirm the importance of CypA antioxidant activity, CypA/P16S was overexpressed in Chang human liver cells and the rate of cell death was measured following treatment with cisplatin or H2O2. Overexpression of CypA/WT protected the cells against cisplatin or H2O2-induced oxidative damage, however, the CypA/P16S mutant had no effect. These findings suggested that CypA exhibits a protective antioxidant effect.</P>

      • Licochalcone A induces apoptosis through endoplasmic reticulum stress via a phospholipase Cγ1-, Ca(2+)-, and reactive oxygen species-dependent pathway in HepG2 human hepatocellular carcinoma cells.

        Choi, A-Young,Choi, Ji Hyun,Hwang, Keun-Young,Jeong, Yeon Ju,Choe, Wonchae,Yoon, Kyung-Sik,Ha, Joohun,Kim, Sung Soo,Youn, Jang Hyun,Yeo, Eui-Ju,Kang, Insug Rapid Science Publishers ; Kluwer Academic Publish 2014 Apoptosis Vol.19 No.4

        <P>Licochalcone A (LicA), an estrogenic flavonoid, induces apoptosis in multiple types of cancer cells. In this study, the molecular mechanisms underlying the anti-cancer effects of LicA were investigated in HepG2 human hepatocellular carcinoma cells. LicA induced apoptotic cell death, activation of caspase-4, -9, and -3, and expression of endoplasmic reticulum (ER) stress-associated proteins, including C/EBP homologous protein (CHOP). Inhibition of ER stress by CHOP knockdown or treatment with the ER stress inhibitors, salubrinal and 4-phenylbutyric acid, reduced LicA-induced cell death. LicA also induced reactive oxygen species (ROS) accumulation and the anti-oxidant N-acetylcysteine reduced LicA-induced cell death and CHOP expression. In addition, LicA increased the levels of cytosolic Ca(2+), which was blocked by 2-aminoethoxydiphenyl borate (an antagonist of inositol 1,4,5-trisphosphate receptor) and BAPTA-AM (an intracellular Ca(2+) chelator). 2-Aminoethoxydiphenyl borate and BAPTA-AM inhibited LicA-induced cell death. Interestingly, LicA induced phosphorylation of phospholipase Cγ1 (PLCγ1) and inhibition of PLCγ1 reduced cell death and ER stress. Moreover, the multi-targeted receptor tyrosine kinase inhibitors, sorafenib and sunitinib, reduced LicA-induced cell death, ER stress, and cytosolic Ca(2+) and ROS accumulation. Finally, LicA induced phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2) and c-Met receptor and inhibition of both receptors by co-transfection with VEGFR2 and c-Met siRNAs reversed LicA-induced cell death, Ca(2+) increase, and CHOP expression. Taken together, these findings suggest that induction of ER stress via a PLCγ1-, Ca(2+)-, and ROS-dependent pathway may be an important mechanism by which LicA induces apoptosis in HepG2 hepatocellular carcinoma cells.</P>

      • KCI등재

        Melatonin prevents doxorubicin-induced cardiotoxicity through suppression of AMPKα2-dependent mitochondrial damage

        양구원,송민혁,HOANG DANG HIEU,TRAN QUYNH HOA,Choe Wonchae,강인숙,김성수,하주헌 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-

        The clinical application of doxorubicin, one of the most effective anticancer drugs, has been limited due to its adverse effects, including cardiotoxicity. One of the hallmarks of doxorubicin-induced cytotoxicity is mitochondrial dysfunction. Despite intensive research over recent decades, there are no effective approaches for alleviating doxorubicin-induced cytotoxicity. Melatonin, a natural hormone that is primarily secreted by the pineal gland, is emerging as a promising adjuvant that protects against doxorubicin-induced cytotoxicity owing to its pharmaceutical effect of preserving mitochondrial integrity. However, the underlying mechanisms are far from completely understood. Here, we provide novel evidence that treatment of H9c2 cardiomyoblasts with doxorubicin strongly induced AMP-activated protein kinase α2 (AMPKα2), which translocated to mitochondria and interfered with their function and integrity, ultimately leading to cellular apoptosis. These phenomena were significantly blocked by melatonin treatment. The levels of AMPKα2 in murine hearts were tightly associated with cardiotoxicity in the context of doxorubicin and melatonin treatment. Therefore, our study suggests that the maintenance of mitochondrial integrity is a key factor in reducing doxorubicin-induced cytotoxicity and indicates that AMPKα2 may serve as a novel target in the design of cytoprotective combination therapies that include doxorubicin.

      • SCISCIESCOPUS

        Alpha-naphthoflavone induces apoptosis through endoplasmic reticulum stress via c-Src-, ROS-, MAPKs-, and arylhydrocarbon receptor-dependent pathways in HT22 hippocampal neuronal cells

        Yu, Ah-Ran,Jeong, Yeon Ju,Hwang, Chi Yeon,Yoon, Kyung-Sik,Choe, Wonchae,Ha, Joohun,Kim, Sung Soo,Pak, Youngmi Kim,Yeo, Eui-Ju,Kang, Insug Elsevier 2019 NeuroToxicology Vol.71 No.-

        <P><B>Abstract</B></P> <P>α-Naphthoflavone (αNF) is a prototype flavone, also known as a modulator of aryl hydrocarbon receptor (AhR). In the present study, we investigated the molecular mechanisms of αNF-induced cytotoxic effects in HT22 mouse hippocampal neuronal cells. αNF induced apoptotic cell death via activation of caspase-12 and -3 and increased expression of endoplasmic reticulum (ER) stress-associated proteins, including C/EBP homologous protein (CHOP). Inhibition of ER stress by treatment with the ER stress inhibitor, salubrinal, or by CHOP siRNA transfection reduced αNF-induced cell death. αNF activated mitogen-activated protein kinases (MAPKs), such as p38, JNK, and ERK, and inhibition of MAPKs reduced αNF-induced CHOP expression and cell death. αNF also induced accumulation of reactive oxygen species (ROS) and an antioxidant, N-acetylcysteine, reduced αNF-induced MAPK phosphorylation, CHOP expression, and cell death. Furthermore, αNF activated c-Src kinase, and inhibition of c-Src by a kinase inhibitor, SU6656, or siRNA transfection reduced αNF-induced ROS accumulation, MAPK activation, CHOP expression, and cell death. Inhibition of AhR by an AhR antagonist, CH223191, and siRNA transfection of AhR and AhR nuclear translocator reduced αNF-induced AhR-responsive luciferase activity, CHOP expression, and cell death. Finally, we found that inhibition of c-Src and MAPKs reduced αNF-induced transcriptional activity of AhR. Taken together, these findings suggest that αNF induces apoptosis through ER stress via c-Src-, ROS-, MAPKs-, and AhR-dependent pathways in HT22 cells.</P> <P><B>Highlights</B></P> <P> <UL> <LI> α-Naphthoflavone (αNF), an arylhydrocarbon receptor modulator (AhR), induces apoptosis in HT22 hippocampal neuronal cells. </LI> <LI> ER stress plays a role in αNF-induced apoptosis. </LI> <LI> The c-Src-, ROS-, MAPK-, and AhR-dependent pathways are implicated in αNF-induced ER stress and apoptosis. </LI> <LI> The AhR nuclear translocator-dependent genomic pathway also mediates αNF-induced ER stress and apoptosis. </LI> </UL> </P>

      • Hydrogen-rich medium protects mouse embryonic fibroblasts from oxidative stress by activating LKB1-AMPK-FoxO1 signal pathway

        Lee, Jihyun,Yang, Goowon,Kim, Young-Joo,Tran, Quynh Hoa,Choe, Wonchae,Kang, Insug,Kim, Sung Soo,Ha, Joohun Elsevier 2017 Biochemical and biophysical research communication Vol.491 No.3

        <P><B>Abstract</B></P> <P>Persistent oxidative stress is recognized as a major cause of many pathological conditions as well as ageing. However, most clinical trials of dietary antioxidants have failed to produce successful outcomes in treating oxidative stress-induced diseases. Molecular hydrogen (H<SUB>2</SUB>) has recently received considerable attention as a therapeutic agent owing to its novel antioxidant properties, a selective scavenger of hydroxyl and peroxynitrite radicals. Beyond this, numerous reports support that H<SUB>2</SUB> can modulate the activity of various cellular signal pathways. However, its effect on AMP-activated protein kinase (AMPK) signal pathway, a central regulator of energy hemostasis, has remained almost elusive. Here, we report that hydrogen-rich medium activated LKB1-AMPK signal pathway without ATP depletion, which in turn induced FoxO1-dependent transcription of manganese superoxide dismutase and catalase in mouse embryonic fibroblasts. Moreover, hydrogen-rich media effectively reduced the level of reactive oxygen species in cells treated with hydrogen peroxide and protected these cells from apoptosis in an AMPK-dependent manner. These results suggest that the LKB1-AMPK-FoxO1 signaling pathway is a critical mediator of the antioxidant properties of H<SUB>2</SUB>, further supporting the idea that H<SUB>2</SUB> acts as a signaling molecule to serve various physiological functions.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Hydrogen-rich medium exerts anti-oxidant effects through AMPK. </LI> <LI> Hydrogen-rich medium activates LKB1-AMPK signal pathway without ATP depletion. </LI> <LI> AMPK in turn induces FoxO1-dependent expression of antioxidant enzymes. </LI> </UL> </P>

      • SCIESCOPUSKCI등재

        Non-Polar Myxococcus fulvus KYC4048 Metabolites Exert Anti-Proliferative Effects via Inhibition of Wnt/β-Catenin Signaling in MCF-7 Breast Cancer Cells

        ( Juha Park ),( Hee-jin Yoo ),( Ah-ran Yu ),( Hye Ok Kim ),( Sang Cheol Park ),( Young Pyo Jang ),( Chayul Lee ),( Wonchae Choe ),( Sung Soo Kim ),( Insug Kang ),( Kyung-sik Yoon ) 한국미생물생명공학회(구 한국산업미생물학회) 2021 Journal of microbiology and biotechnology Vol.31 No.4

        The Wnt/β-catenin signaling pathway is involved in breast cancer and Myxococcus fulvus KYC4048 is a myxobacterial strain that can produce a variety of bioactive secondary metabolites. Although a previous study revealed that KYC4048 metabolites exhibit anti-proliferative effects on breast cancer, the biochemical mechanism involved in their effects remains unclear. In the present study, KYC4048 metabolites were separated into polar and non-polar (ethyl acetate and n-hexane) fractions via liquid-liquid extraction. The effects of these polar and non-polar KYC4048 metabolites on the viability of breast cancer cells were then determined by MTT assay. Expression levels of Wnt/ β-catenin pathway proteins were determined by Western blot analysis. Cell cycle and apoptosis were measured via fluorescence-activated cell sorting (FACS). The results revealed that non-polar KYC4048 metabolites induced cell death of breast cancer cells and decreased expression levels of WNT2B, β-catenin, and Wnt target genes (c-Myc and cyclin D1). Moreover, the n-hexane fraction of non-polar KYC4048 metabolites was found most effective in inducing apoptosis, necrosis, and cell cycle arrest, leading us to conclude that it can induce apoptosis of breast cancer cells through the Wnt/β-catenin pathway. These findings provide evidence that the n-hexane fraction of non-polar KYC4048 metabolites can be developed as a potential therapeutic agent for breast cancer via inhibition of the Wnt/β-catenin pathway.

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