New cinnamate group-containing copolymers for a self-curable, humidity-sensitive polyelectrolyte and polymeric anchoring agents were prepared by copolymerization of [2-[(methacryloyloxy) ethyl]dimethyl]propyl ammonium bromide(MEPAB), methyl methacrylate(MMA), 3-(trimethoxysilyl) propyl methacrylate(TMSPM) and 2-(cinnamoyloxy)ethyl methacrylate(CEMA). Photocrosslinkable copolymer composed of MEPAB/MMA/TMSPM/CEMA=70/20/0/10 were used for humidity-sensitive membrane, and those of 50/0/20/30 and 0/0/50/50 were used for polymeric anchoring agents. 3- (Triethoxysilyl)propyl cinnamate(TESPC) was also used as a surface-pretreating agent for the comparison of capability of attachment of polyelectrolyte to the electrode surface with polymeric photocurable silanecoupling agents. Pretreatment of the electrode substrate with anchoring agents was performed to form a cinnamate thin film on the electrode through covalent bonds. When the sensors were irradiated with UV light, the anchoring of a polyelectrolyte into the substrate was carried out via the [2$\pi$+2$\pi$] cycloaddition. The resulting sensors using polymeric anchoring agents and TESPC showed water durability with increase of resistance by 60~85%, which is corresponding to the reduction of 2.25~3.15%RH, after soaking in water for 24 h. They showed good hysteresis (-0.2%RH), response time (90 sec) and long-term stability at high temperature and humidity.
$I{\kappa}B$, a cytoplasmic inhibitor of nuclear factor-${\kappa}B$ ($NF-{\kappa}B$), is reportedly degraded via the proteasome. However, we recently found that long-term incubation with proteasome inhibitors (PIs) such as PS-341 or MG132 induces $I{\kappa}B{\alpha}$ degradation via an alternative pathway, lysosome, which results in $NF-{\kappa}B$ activation and confers resistance to PI-induced lung cancer cell death. To enhance the anti-cancer efficacy of PIs, elucidation of the regulatory mechanism of PI-induced $I{\kappa}B{\alpha}$ degradation is necessary. Here, we demonstrated that PI up-regulates nuclear factor (erythroid-derived 2)-like 2 (Nrf2) via both de novo protein synthesis and Kelch-like ECH-associated protein 1 (KEAP1) degradation, which is responsible for $I{\kappa}B{\alpha}$ degradation via macroautophagy activation. PIs increased the protein level of light chain 3B (LC3B, macroautophagy marker), but not lysosome-associated membrane protein 2a (Lamp2a, the receptor for chaperone-mediated autophagy) in NCI-H157 and A549 lung cancer cells. Pretreatment with macroautophagy inhibitor or knock-down of LC3B blocked PI-induced $I{\kappa}B{\alpha}$ degradation. PIs up-regulated Nrf2 by increasing its transcription and mediating degradation of KEAP1 (cytoplasmic inhibitor of Nrf2). Overexpression of dominant-negative Nrf2, which lacks an N-terminal transactivating domain, or knock-down of Nrf2 suppressed PI-induced LC3B protein expression and subsequent $I{\kappa}B{\alpha}$ degradation. Thus, blocking of the Nrf2 pathway enhanced PI-induced cell death. These findings suggest that Nrf2-driven induction of LC3B plays an essential role in PI-induced activation of the $I{\kappa}B$/$NF-{\kappa}B$ pathway, which attenuates the anti-tumor efficacy of PIs.
Chung, Hak Jae;Sa, Soo Jin;Baek, Sun Young;Cho, Eun Suek;Kim, Young Shin;Hong, Jun Ki;Cho, Kyu Ho;Kim, Ji Youn;Park, Mi Ryung;Kim, Kyung Woon
Journal of the Korea Academia-Industrial cooperation Society
/
v.20
no.9
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pp.306-314
/
2019
As dipeptidyl peptidase-4(DPP-4) inhibitors are used widely as a secondary treatment for type 2 diabetes because they tend to be well tolerated with minimal side effects, the human DPP-4(hDPP-4) gene was injected into a pig zygote through micro-injection, and 1-cell stage fertilized embryos were then transplanted surgically into the oviduct. Three pigs were fertilized with hDPP-4 genes and produced sixteen piglets, in which one male piglet was identified to be transgenic. Finally, transgenic pigs showing hDPP-4 gene expression in the tail were produced. Western blot and RT-PCR analysis confirmed that the hDPP-4 is expressed strongly in the membrane cells of the transgenic pig, and that the hDPP-4 gene appears in various tissues and tails. This suggests that the expression vector is normally expressed in transgenic pigs. These results are anticipated to be a model animal to check the endocrine function for insulin resistance that occurs in a hDPP-4 transgenic pig and to increase its value for use as a material in newly developed medicines.
Glioblastoma is the most common primary malignant brain tumor and has an extremely poor prognosis. Glioblastoma stem cells (GSCs) contribute to tumor initiation, recurrence, and resistance to therapy, and are thus a key therapeutic target. The peel of Citrus unshiu Markovich has been used in traditional medicine in East Asia to treat various diseases. In this study, we investigated the anticancer activity and molecular mechanism of the chloroform extract of this natural product (CECU) in U87MG GSCs. The results show that CECU inhibited the proliferation, tumorsphere formation, and migration of U87MG GSCs by causing cell cycle arrest at the G0/G1 phase and apoptosis. In addition, CECU downregulated key cancer stemness regulators, including CD133, Oct4, Nanog, integrin α6, ALDH1A1, and STAT3 signaling in U87MG GSCs. Furthermore, CECU significantly suppressed in vivo tumor growth of U87MG GSCs in a chorioallantoic membrane model. Therefore, CECU can be utilized as a natural medicine for the prevention and treatment of glioblastoma.
Eun Mi Hwang;Bo Hyun Lee;Eun Hye Byun;Soomin Lee;Dawon Kang;Dong Kun Lee;Min Seok Song;Seong-Geun Hong
The Korean Journal of Physiology and Pharmacology
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v.27
no.4
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pp.417-426
/
2023
The TRPM4 gene encodes a Ca2+-activated monovalent cation channel called transient receptor potential melastatin 4 (TRPM4) that is expressed in various tissues. Dysregulation or abnormal expression of TRPM4 has been linked to a range of diseases. We introduced the hemagglutinin (HA) tag into the extracellular S6 loop of TRPM4, resulting in an HA-tagged version called TRPM4-HA. This TRPM4-HA was developed to investigate the purification, localization, and function of TRPM4 in different physiological and pathological conditions. TRPM4-HA was successfully expressed in the intact cell membrane and exhibited similar electrophysiological properties, such as the current-voltage relationship, rapid desensitization, and current size, compared to the wild-type TRPM4. The presence of the TRPM4 inhibitor 9-phenanthrol did not affect these properties. Furthermore, a wound-healing assay showed that TRPM4-HA induced cell proliferation and migration, similar to the native TRPM4. Co-expression of protein tyrosine phosphatase, non-receptor type 6 (PTPN6 or SHP1) with TRPM4-HA led to the translocation of TRPM4-HA to the cytosol. To investigate the interaction between PTPN6 and tyrosine residues of TRPM4 in enhancing channel activity, we generated four mutants in which tyrosine (Y) residues were substituted with phenylalanine (F) at the N-terminus of TRPM4. The YF mutants displayed properties and functions similar to TRPM4-HA, except for the Y256F mutant, which showed resistance to 9-phenanthrol, suggesting that Y256 may be involved in the binding site for 9-phenanthrol. Overall, the creation of HA-tagged TRPM4 provides researchers with a valuable tool to study the role of TRPM4 in different conditions and its potential interactions with other proteins, such as PTPN6.
Methela Nusrat Jahan;Islam Mohammad Shafiqul;Da-Sol Lee;Youn-Ji Woo;Bong-Gyu Mun;Byung-Wook Yun
Proceedings of the Korean Society of Crop Science Conference
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2023.04a
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pp.105-105
/
2023
Heavy metals, including lead (Pb) toxicity, are increasing in soil and are considered toxic in small amounts. Pb contamination is mainly caused by industrialization - smelting, mining. Agricultural practices - sewage sludge, pests and urban practices - lead paint. It can seriously damage and threaten crop growth. Pb can adversely affect plant growth and development by affecting the photosystem, cell membrane integrity, and excessive production of reactive oxygen species (ROS) such as hydrogen peroxide (H2O2)andsuperoxide(O2.-). NO is produced via enzymatic and non-enzymatic antioxidants to scavenge ROS and lipid peroxidation substrates in terms of protecting cells from oxidative damage. Thus, NO improves ion homeostasis and confers resistance to metal stress. Our results here suggest that exogenous NO may aid in better growth under lead stress. These enhancements may be aided by NO's ability in sensing, signaling and stress tolerance in plants under heavy metal stress in combination with lead stress. Our results show that GSNO has a positive effect on soybean seedling growth in response to axillary pressure and that NO supplementation helps to reduce chlorophyll maturation and relative water content in leaves and roots following strong burst under lead stress. GSNO supplementation (200 µM and 100 µM) reduced compaction and approximated oxidative damage of MDA, proline and H2O2. Under plant tension, a distorted appearance was found in the relief of oxidative damage by ROS scavenging by GSNO application. In summary, modulation of these NO, PCS and prolongation of metal past reversing GSNO application confirms the detoxification of ROS induced by toxic metal rates in soybean. In summary, these NO, PCS and metal traditionally sustained rates of reverse GSNO application confirm the detoxification of ROS induced by toxic metal rates in soybean.
Licochalcone C (LCC; PubChem CID:9840805), a chalcone compound originating from the root of Glycyrrhiza inflata, has shown anticancer activity against skin cancer, esophageal squamous cell carcinoma, and oral squamous cell carcinoma. However, the therapeutic potential of LCC in treating colorectal cancer (CRC) and its underlying molecular mechanisms remain unclear. Chemotherapy for CRC is challenging because of the development of drug resistance. In this study, we examined the antiproliferative activity of LCC in human colorectal carcinoma HCT116 cells, oxaliplatin (Ox) sensitive and Ox-resistant HCT116 cells (HCT116-OxR). LCC significantly and selectively inhibited the growth of HCT116 and HCT116-OxR cells. An in vitro kinase assay showed that LCC inhibited the kinase activities of EGFR and AKT. Molecular docking simulations using AutoDock Vina indicated that LCC could be in ATP-binding pockets. Decreased phosphorylation of EGFR and AKT was observed in the LCC-treated cells. In addition, LCC induced cell cycle arrest by modulating the expression of cell cycle regulators p21, p27, cyclin B1, and cdc2. LCC treatment induced ROS generation in CRC cells, and the ROS induction was accompanied by the phosphorylation of JNK and p38 kinases. Moreover, LCC dysregulated mitochondrial membrane potential (MMP), and the disruption of MMP resulted in the release of cytochrome c into the cytoplasm and activation of caspases to execute apoptosis. Overall, LCC showed anticancer activity against both Ox-sensitive and Ox-resistant CRC cells by targeting EGFR and AKT, inducing ROS generation and disrupting MMP. Thus, LCC may be potential therapeutic agents for the treatment of Ox-resistant CRC cells.
Purpose: Uptakes of Tc-99m MIBI (MIBI) and Tc-99m tetrofosmin (tetrofosmin) in human non-small cell lung cancer A549, multidrug-resistance associated protein (MRP) expressing cell, were investigated in vitro and in vivo. Materials and Methods: Western blot analysis and immunohistochemistry were used for detection of MRP in A549 cells with anti-MRPr1 antibody. Cellular uptakes of two tracers were evaluated at $100{\mu}M$ of verapamil (Vrp), $50{\mu}M$ of cyclosporin A (CsA) and $25{\mu}M$ of butoxysulfoximide (BSO) after incubation with MIBI and tetrofosmin for 30 and 50 min at $37^{\circ}C$, using single cell suspensions at $1{\times}10^6cells/ml$. Radioactivities in supernatants and pellets were measured with gamma well counter. A549 cells were inoculated in each flanks of 24 nude mice. Group 1 (Gr1) and Gr3 mice were treated with only MIBI or tetrofosmin, and Gr2 and Gr4 mice were treated with 70mg/kg of CsA i.p. for 1 hour before injection of 370KBq of MIBI or tetrofosmin. Mice were sacrificed at 10, 60 and 240 min. Radioactivities of organs and tumors were expressed as percentage injected dose per gram of tissue (%ID/gm). Results: Western blot analysis of the A549 cells detected expression of MRPr1 (190 kDa) and immunohistochemical staining of tumor tissue for MRPr1 revealed brownish staining in cell membrane but not P-gp. Upon incubating A549 cells for 60 min with MIBI and tetrofosmin, cellular uptake of MIBI was higher than that of tetrofosmin. Coincubation with modulators resulted in an increase in cellular uptakes of MIBI and tetrofosmin. Percentage increase of MIBI was higher than that of tetrofosmin with Vrp by 623% and 427%, CsA by 753% and 629% and BSO by 219% and 140%, respectively. There was no significant difference in tumoral uptakes of MIBI and tetrofosmin between Gr1 and Gr3. Percentage increases in MIBI (114% at 10 min, 257% at 60 min, 396% at 240 min) and tetrofosmin uptake (110% at 10 min, 205% at 60 min, 410% at 240 min) were progressively higher by the time up to 240 min with CsA. Conclusion: These results indicate that MIBI and tetrofosmin are suitable tracers for imaging MRP-mediated drug resistance in A549 tumors. MIBI may be a better tracer than tetrofosmin for evaluating MRP reversal effect of modulators.
Purpose : Infection with Shiga-like toxin (SLT)-producing Escherichia coli, an emerging human pathogen found particularly in young children under 5 years of age, causes a spectrum of illnesses with high morbidity and mortality, ranging from diarrhea to hemorrhagic colitis and hemolytic uremic syndrome. Host mediators play an important role in the pathogenesis of SLT-I toxicity. The experiments described here were designed to investigate the effect of SLT-I on TNF-${\alpha}$ production and to understand the effect of TNF-${\alpha}$ on GB3 expression. We also further examine the relationship between the Gb3 level and the differential susceptibility of cells to the cytotoxic action of SLT-I. Methods : The effect of purified SLT-1 from E. coli O157 : H7 (ATCC 43890) on tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) production in Raw264.7 cells was investigated. Many mediators regulate endothelial cell membrane expression of the glycolipid globotriaosyleramide (Gb3), which serves as the toxin receptor, suggesting that the host response to the toxin or other bacterial products may contribute to pathogenesis by regulating target cell sensitivity to the toxins. Therefore, the relationships between Gb3 expression and cytotoxicity against SLT-I on three types of cells were evaluated. Results : Detectable levels of TNF-${\alpha}$ were produced as early as six hours after induction and continued to increase during 48 hours by SLT-I. It was also found that Vero cells and dendritic cells (DC2.4 cells) expressed high levels of Gb3, 83% and 68%, respectively, and that Raw264.7 cells had a low level of Gb3 (29%) and appeared refractory to cytotoxicity against SLT-I. Vero cells and DC2.4 cells expressing high levels of Gb3 were highly susceptible to SLT-I. Furthermore, macrophages showed a resistance to SLT-I cytotoxicity, despite the fact that Gb3 expression was enhanced. Conclusion : These results strongly suggest that the expression of Gb3 is necessary but not sufficient to confer sensitivity of macrophages to SLT-I and further underpin the important role of SLT-I and its Gb3 receptors in the pathogenesis of E. coli O157 infection.
Breslau's report on the two stillbirths induced by illuminating gas poisoning made many investigators explore the hazards. of carbon monoxide(CO) poisoning to pregnancy. The pregnant woman, her fetus, and the newborn infant have been identified to be particularly vulnerable to CO even in low concentration. Several factors, such as placental barrier, membrane resistance of maternal and fetal red blood cells etc., were considered to be related to the delayed elimination of CO from fetus. Slower elimination of CO from fetus than from mother was confirmed in several in vivo studies. But there are few studies which have confirmed the difference of carboxyhemoglobin (HbCO) dissociation in adult and fetal bloods. Author investigated the effects of hemoglobin itself on the elimination of CO from mother and fetus. By observing the difference of CO dissociation from adult and fetal hemoglobin at the various partial pressures of oxygen, the author tries to suggest the base of the proper treatment measure for the CO poisoning of pregnant woman and newborn infant. The results were as follows: 1. The total hemoglobin amounts of adults and fetal bloods were $16.1{\pm}0.50gm%\;and\;15.7{\pm}0.32gm%$, respectively. The fetal hemoglobin proportions in adult and fetal bloods were $1.2{\pm}0.15%\;and\;72.7{\pm}3.01%$, respectively. 2. Adult and fetal bloods saturated by CO to 100% HbCO were exposed to ambient air$(21%\;O_2),\;100%\;O_2\;and\;3\;ATAO_2$. After 30 minutes exposure, the HbCO saturations of adult blood were 96.7%, 70.9%, and 52.8%, respectively, and those of fetal blood were 98.5%, 76.1%, and 62.2%, respectively. HbCO dissociation was proportional to the partial pressure of oxygen and the most marked dissociation was shown under 3 ATA $O_2$, HbCO dissociation of fetal blood was slower than that of adult blood in all conditions. According to the above results, it is possible that CO poisoning make more serious damage to the fetus and newborn infant than to the adult due to the delayed dissociation of HbCO. Thus in the treatment of CO poisoning of pregnant woman and newborn infant, hyperbaric oxygen therapy seems to be the most eflective treatment measure, but the duration of hyperbaric oxygenation should be lengthened accordingly.
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