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| 1 | Glycer-AGEs-RAGE signaling enhances the angiogenic potential of hepatocellular carcinoma by upregulating VEGF expression显示文摘AIM:To investigate the effect of glyceraldehyde-derived advanced glycation end-products(Glycer-AGEs) on hepatocellular carcinoma(HCC)cells.METHODS:Two HCC cell lines(Hep3B and HepG2 cells)and human umbilical vein endothelial cells(HUVEC)were used.Cell viability was determined using the WST-8 assay.Western blotting,enzyme linked immunosorbent assay,and real-time reverse transcriptionpolymerase chain reactions were used to detect protein and mRNA.Angiogenesis was evaluated by assessing the proliferation,migration,and tube formation of HUVEC.RESULTS:The receptor for AGEs(RAGE)protein was detected in Hep3B and HepG2 cells.HepG2 cells werenot affected by the addition of Glycer-AGEs.GlycerAGEs markedly increased vascular endothelial growth factor(VEGF)mRNA and protein expression,which is one of the most potent angiogenic factors.Compared with the control unglycated bovine serum albumin(BSA) treatment,VEGF mRNA expression levels induced by the Glycer-AGEs treatment were 1.00±0.10 vs 1.92 ±0.09(P<0.01).Similarly,protein expression levels induced by the Glycer-AGEs treatment were 1.63±0.04 ng/mL vs 2.28±0.17 ng/mL for the 24 h treatment and 3.36±0.10 ng/mL vs 4.79±0.31 ng/mL for the 48 h treatment,respectively(P<0.01).Furthermore,compared with the effect of the control unglycated BSA-treated conditioned medium,the Glycer-AGEstreated conditioned medium significantly increased the proliferation,migration,and tube formation of HUVEC,with values of 122.4%±9.0%vs 144.5%±11.3%for cell viability,4.29±1.53 vs 6.78±1.84 for migration indices,and 71.0±7.5 vs 112.4±8.0 for the number of branching points,respectively(P<0.01).CONCLUSION:These results suggest that Glycer-AGEs-RAGE signaling enhances the angiogenic potential of HCC cells by upregulating VEGF expression. | Junichi Takino Shoichi Yamagishi Masayoshi Takeuchi | 2012 | World Journal of Gastroenterology2012，18，15： | 27 |
| 2 | MK615 decreases RAGE expression and inhibits TAGE-induced proliferation in hepatocellular carcinoma cells显示文摘AIM:To investigate the proliferative effect of advanced glycation end-products(AGEs) and the role of their cellular receptor(RAGE) on hepatocellular carcinoma(HCC) cells,and the inhibitory effects of MK615,an extract from Japanese apricot,against AGEs were also evaluated.METHODS:Two HCC cell lines,HuH7 and HepG2,were used.Expression of RAGE was investigated by poly-merase chain reaction,Western blotting,and flow cytemetry(FACS).The effect of MK615 on RAGE expression was also evaluated by FACS.The proliferative effects of a control(unglycated bovine serum albumin),glucosederived AGEs(Glc-AGE),and glyceraldehyde-derived AGEs(Glycer-AGE),and the anti-proliferative effect of MK615 against AGEs,were evaluated using MTT assays.RESULTS:Expression of RAGE was confirmed at both the mRNA and protein levels in both HuH7 and HepG2.FACS revealed that the level of RAGE expression was higher in HuH7 than in HepG2.Treatment with 0.1 μg/mL MK615 decreased the expression level of RAGE from 24.3% to 3.7% in HuH7 and from 6.2% to 4.8% in HepG2.The growth indices for the control,Glc-AGE,and Glycer-AGE were 1.06 ± 0.08,0.99 ± 0.04,and 1.38 ± 0.05,respectively,in HuH7(P = 0.037),and were 1.03 ± 0.04,1.04 ± 0.03,and 1.07 ± 0.05,respectively,in HepG2(P > 0.05).When the cells were cultured simultaneously with Glycer-AGE and MK615,MK615 abrogated the proliferative effect of Glycer-AGE in HuH7.CONCLUSION:Only Glycer-AGE has a proliferative effect on HuH7,which expresses a higher level of RAGE.MK615 suppresses the proliferative effect of GlycerAGE on HuH7 by decreasing the expression of RAGE. | Yuhki Sakuraoka Tokihiko Sawada Toshie Okada Takayuki Shiraki Yoshikazu Miura Katsuya Hiraishi Tatsushi Ohsawa Masakazu Adachi Jun-ichi Takino Masayoshi Takeuchi Keiichi Kubota | 2010 | World Journal of Gastroenterology2010，16，42： | 6 |
| 3 | Involvement of the TAGE-RAGE system in non-alcoholic steatohepatitis: Novel treatment strategies显示文摘Non-alcoholic fatty liver disease(NAFLD)is a major cause of liver disease around the world.It includes a spectrum of conditions from simple steatosis to non-alcoholic steatohepatitis(NASH)and can lead to fibrosis,cirrhosis,liver failure,and/or hepatocellular carcinoma.NAFLD is also associated with other medical conditions such as obesity,diabetes mellitus(DM),metabolic syn-drome,hypertension,insulin resistance,hyperlipidemia,and cardiovascular disease(CVD).In diabetes,chronic hyperglycemia contributes to the development of both macro-and microvascular conditions through a variety of metabolic pathways.Thus,it can cause a variety of metabolic and hemodynamic conditions,including upregulated advanced glycation end-products(AGEs)synthesis.In our previous study,the most abundant type of toxic AGEs(TAGE);i.e.,glyceraldehyde-derived AGEs,were found to make a significant contribution to the pathogenesis of DM-induced angiopathy.Furthermore,accumulating evidence suggests that the binding of TAGE with their receptor(RAGE)induces oxidative damage,promotes inflammation,and causes changes in intracellular signaling and the expression levels of certain genes in various cell populations including hepatocytes and hepatic stellate cells.All of these effects could facilitate the pathogenesis of hypertension,cancer,diabetic vascular complications,CVD,dementia,and NASH.Thus,inhibiting TAGE synthesis,preventing TAGE from binding to RAGE,and downregulating RAGE expression and/or the expression of associated effector molecules all have potential as therapeutic strategies against NASH.Here,we examine the contributions of RAGE and TAGE to various conditions and novel treatments that target them in order to prevent the development and/or progression of NASH. | Masayoshi Takeuchi Jun-ichi Takino Akiko Sakasai-Sakai Takanobu Takata Tadashi Ueda Mikihiro Tsutsumi Hideyuki Hyogo Sho-ichi Yamagishi | 2014 | World Journal of Hepatology2014，6，12： | 5 |
| 4 | Contribution of the toxic advanced glycation end-productsreceptor axis in nonalcoholic steatohepatitis-related hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC) is one of the most common malignancies worldwide. The main etiologies of HCC are hepatitis B virus and hepatitis C virus(HCV), and non-hepatitis B/non-hepatitis C HCC(NBNCHCC) has also been identified as an etiological factor. Although the incidence of HCV-related HCC in Japan has decreased slightly in recent years, that of NBNC-HCC has increased. The onset mechanism of NBNC-HCC, which has various etiologies, remains unclear; however, nonalcoholic steatohepatitis(NASH), a severe form of nonalcoholic fatty liver disease, is known to be an important risk factor for NBNC-HCC. Among the different advanced glycation end-products(AGEs) formed by the Maillard reaction, glyceraldehyde-derived AGEs, the predominant components of toxic AGEs(TAGE), have been associated with NASH and NBNC-HCC, including NASH-related HCC. Furthermore, the expression of the receptor for AGEs(RAGE) has been correlated with the malignant progression of HCC. Therefore, TAGE induce oxidative stress by binding with RAGE may, in turn, lead to adverse effects, such as fibrosis and malignant transformation, in hepatic stellate cells and tumor cells during NASH or NASH-related HCC progression. The aim of this review was to examine the contribution of the TAGE-RAGE axis in NASH-related HCC. | Jun-ichi Takino Kentaro Nagamine Takamitsu Hori Akiko Sakasai-Sakai Masayoshi Takeuchi | 2015 | World Journal of Hepatology2015，7，23： | 4 |
| 5 | Atorvastatin decreases serum levels of advanced glycation endproducts (AGEs) in nonalcoholic steatohepatitis (NASH) patients with dyslipidemia: clinical usefulness of AGEs as a biomarker for the attenuation of NASH显示文摘 | Yuki Kimura Hideyuki Hyogo Sho-ichi Yamagishi Masayoshi Takeuchi Tomokazu Ishitobi Yoshitaka Nabeshima Koji Arihiro Kazuaki Chayama | 2010 | Journal of Gastroenterology2010，，7： | 3 |
| 6 | Glucagon-like peptide-1 (GLP-1) inhibits advanced glycation end product (AGE)-induced up-regulation of VCAM-1 mRNA levels in endothelial cells by suppressing AGE receptor (RAGE) expression显示文摘 | Yuji Ishibashi Takanori Matsui Masayoshi Takeuchi Sho-ichi Yamagishi | 2009 | Biochemical and Biophysical Research Communications2009，，3： | 2 |
| 7 | Long-term outcomes after a variety of video-assisted thoracoscopic lobectomy approaches for clinical stage IA lung cancer: A multi-institutional study显示文摘 | Norihisa Shigemura Akinori Akashi Soichiro Funaki Tomoyuki Nakagiri Masayoshi Inoue Noriyoshi Sawabata Hiroyuki Shiono Masato Minami Yukiyasu Takeuchi Meinoshin Okumura Yoshiki Sawa | 2006 | The Journal of Thoracic and Cardiovascular Surgery2006，，3： | 2 |
| 8 | The formation of intracellular glyceraldehyde-derived advanced glycation end-products and cytotoxicity显示文摘 | Jun-ichi Takino Yuka Kobayashi Masayoshi Takeuchi | 2010 | Journal of Gastroenterology2010，，6： | 1 |
| 9 | Advanced Glycation Endproduct-Induced Calcium Handling Impairment in Mouse Cardiac Myocytes显示文摘 | Ralica Petrova Yasuhiko Yamamoto Katsuhiko Muraki Hideto Yonekura Shigeru Sakurai Takuo Watanabe Hui Li Masayoshi Takeuchi Zenji Makita Ichiro Kato Shin Takasawa Hiroshi Okamoto Yuji Imaizumi Hiroshi Yamamoto | 2002 | Journal of Molecular and Cellular Cardiology2002，，10： | 1 |
| 10 | Atorvastatin decreases serum levels of advanced glycation endproducts (AGEs) in nonalcoholic steatohepatitis (NASH) patients with dyslipidemia: clinical usefulness of AGEs as a biomarker for the attenuation of NASH显示文摘 | Yuki Kimura Hideyuki Hyogo Sho-ichi Yamagishi Masayoshi Takeuchi Tomokazu Ishitobi Yoshitaka Nabeshima Koji Arihiro Kazuaki Chayama | 2010 | Journal of Gastroenterology2010，，7： | 1 |
| 11 | In vitro identification of nonalcoholic fatty liver diseaserelated protein hnRNPM显示文摘AIM:To study the formation of intracellular glyceraldehyde-derived advanced glycation end products(Glycer-AGEs)in the presence of high concentrations of fructose.METHODS:Cells of the human hepatocyte cell line Hep3B were incubated with or without fructose for five days,and the corresponding cell lysates were separated by two-dimensional gradient sodium dodecyl sulfate-polyacrylamide gel electrophoresis.Glycer-AGEs were detected with the anti-Glycer-AGEs antibody.Furthermore,the identification of the proteins that are modified by glyceraldehyde in the presence of high concentrations of fructose was conducted using matrixassisted laser desorption/ionization time-of-flight mass spectrometry(MALDI-TOF-MS).The protein and m RNA levels were determined by Western blotting and realtime reverse transcription PCR,respectively.RESULTS:The results of the two-dimensional gradient sodium dodecyl sulfate-polyacrylamide gel electrophoresis indicated a greater amount of GlycerAGEs in the sample exposed to high concentrations of fructose than in the control.The detected GlycerAGEs showed isoelectric points in the range of 8.0-9.0and molecular weights in the range of 60-80 k Da.The heterogeneous nuclear ribonucleoprotein M(hn RNPM),which plays an important role in regulating gene expression by processing heterogeneous nuclear RNAs to form mature m RNAs,was identified as a modified protein using MALDI-TOF-MS.Increasing the concentration of fructose in the medium induced a concentration-dependent increase in the generated Glycer-AGEs.Furthermore,in an experiment using glyceraldehyde,which is a precursor of Glycer-AGEs,hn RNPM was found to be more easily glycated than the other proteins.CONCLUSION:The results suggest that glyceraldehyde-modified hn RNPM alters gene expression.This change may cause adverse effects in hepatocytes and may serve as a target for therapeutic intervention. | Jun-ichi Takino Kentaro Nagamine Masayoshi Takeuchi Takamitsu Hori | 2015 | World Journal of Gastroenterology2015，21，6： | 1 |
| 12 | Argon plasma coagulation treatment of hemorrhagic radiation proctopathy: the optimal settings for application and long-term outcome显示文摘 | Yasushi Sato Tetsuji Takayama Tamotsu Sagawa Masahiro Hirakawa Hiroyuki Ohnuma Koji Miyanishi Tsutomu Sato Rishu Takimoto Masayoshi Kobune Koichi Okamoto Hisashi Takeuchi Junji Kato | 2011 | Gastrointestinal Endoscopy2011，，： | 1 |
| 13 | Nifedipine, a calcium channel blocker, inhibits advanced glycation end product (AGE)-elicited mesangial cell damage by suppressing AGE receptor (RAGE) expression via peroxisome proliferator-activated receptor-gamma activation显示文摘 | Takanori Matsui Sho-ichi Yamagishi Masayoshi Takeuchi Seiji Ueda Kei Fukami Seiya Okuda | 2009 | Biochemical and Biophysical Research Communications2009，，2： | 1 |
| 14 | Pravastatin inhibits advanced glycation end products (AGEs)-induced proximal tubular cell apoptosis and injury by reducing receptor for AGEs (RAGE) level显示文摘 | Yuji Ishibashi Sho-ichi Yamagishi Takanori Matsui Keisuke Ohta Ryuichiro Tanoue Masayoshi Takeuchi Seiji Ueda Kei-ichiro Nakamura Seiya Okuda | 2012 | Metabolism2012，，8： | 1 |
| 15 | Expression of Muscarinic Receptor Subtypes in Rat Gastric Smooth Muscle显示文摘 | Masayoshi Kajimura Ken Takeuchi | 1997 | Digestive Diseases and Sciences1997，42，5： | 1 |
| 16 | DNA Aptamer Raised Against AGEs Blocks the Progression of Experimental Diabetic Nephropathy显示文摘 | Yusuke Kaida Kei Fukami Takanori Matsui Yuichiro Higashimoto Yuri Nishino Nana Obara Yosuke Nakayama Ryotaro Ando Maki Toyonaga Seiji Ueda Masayoshi Takeuchi Hiroyoshi Inoue Seiya Okuda Sho-ichi Yamagishi | 2013 | Diabetes2013，，9： | 1 |
| 17 | The usefulness of CEA and/or CA19-9 in monitoring for recurrence in gastric cancer patients: a prospective clinical study显示文摘 | Yutaka Takahashi Tetsuo Takeuchi Junichi Sakamoto Tetsuya Touge Masayoshi Mai Hisanao Ohkura Susumu Kodaira Kunio Okajima Hiroaki Nakazato | 2003 | Gastric Cancer2003，，3： | 1 |
| 18 | Advanced glycation end products attenuate cellular insulin sensitivity by increasing the generation of intracellular reactive oxygen species in adipocytes显示文摘 | Hiroyuki Unoki Hideaki Bujo Sho-ichi Yamagishi Masayoshi Takeuchi Tsutomu Imaizumi Yasushi Saito | 2006 | Diabetes Research and Clinical Practice2006，，2： | 1 |
| 19 | Volatile Comstituents of Calamondin Peel and Juice (Citrus madurensis Lour) Cultivated in the Philippines显示文摘 | Hiroaki Takeuchi Yoshihito Ubukata Masayoshi Hanafusa | 2005 | J Essent Oil Res2005，17，： | 1 |
| 20 | Reduced cell replication and induction of apoptosis by advanced glycation end products in rat Schwann cells显示文摘 | Hiromi Sekido Takeshi Suzuki Takahito Jomori Masayoshi Takeuchi Chihiro Yabe-Nishimura Soroku Yagihashi | 2004 | Biochemical and Biophysical Research Communications2004，，1： | 1 |
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