17 results on '"Che, Yi"'
Search Results
2. A non-genetic engineering platform for rapidly generating and expanding cancer-specific armed T cells
- Author
-
Yi-Jou Chen, Michael Chen, Tian-Lu Cheng, Yi-Shan Tsai, Chang-Hung Wang, Che-Yi Chen, Tung-Yun Wu, Shey-Cherng Tzou, Kai-Hung Wang, Jing-Jy Cheng, An-Pei Kao, Shyr-Yi Lin, and Kuo-Hsiang Chuang
- Subjects
Adoptive T cell therapy ,Cancer-specific T cell ,Bispecific antibody (BsAb) ,Virus-free engineering platform ,BsAb-armed T cell ,Medicine - Abstract
Abstract Background Cancer-specific adoptive T cell therapy has achieved successful milestones in multiple clinical treatments. However, the commercial production of cancer-specific T cells is often hampered by laborious cell culture procedures, the concern of retrovirus-based gene transfection, or insufficient T cell purity. Methods In this study, we developed a non-genetic engineering technology for rapidly manufacturing a large amount of cancer-specific T cells by utilizing a unique anti-cancer/anti-CD3 bispecific antibody (BsAb) to directly culture human peripheral blood mononuclear cells (PBMCs). The anti-CD3 moiety of the BsAb bound to the T cell surface and stimulated the differentiation and proliferation of T cells in PBMCs. The anti-cancer moiety of the BsAb provided these BsAb-armed T cells with the cancer-targeting ability, which transformed the naïve T cells into cancer-specific BsAb-armed T cells. Results With this technology, a large amount of cancer-specific BsAb-armed T cells can be rapidly generated with a purity of over 90% in 7 days. These BsAb-armed T cells efficiently accumulated at the tumor site both in vitro and in vivo. Cytotoxins (perforin and granzyme) and cytokines (TNF-α and IFN-γ) were dramatically released from the BsAb-armed T cells after engaging cancer cells, resulting in a remarkable anti-cancer efficacy. Notably, the BsAb-armed T cells did not cause obvious cytokine release syndrome or tissue toxicity in SCID mice bearing human tumors. Conclusions Collectively, the BsAb-armed T cell technology represents a simple, time-saving, and highly safe method to generate highly pure cancer-specific effector T cells, thereby providing an affordable T cell immunotherapy to patients.
- Published
- 2023
- Full Text
- View/download PDF
3. Klf8 regulates left-right asymmetric patterning through modulation of Kupffer’s vesicle morphogenesis and spaw expression
- Author
-
Che-Yi Lin, Ming-Yuan Tsai, Yu-Hsiu Liu, Yu-Fen Lu, Yi-Chung Chen, Yun-Ren Lai, Hsin-Chi Liao, Huang-Wei Lien, Chung-Hsiang Yang, Chang-Jen Huang, and Sheng-Ping L. Hwang
- Subjects
Zebrafish ,Klf8 ,Spaw ,L-R patterning ,Kupffer’s vesicle ,Medicine - Abstract
Abstract Background Although vertebrates are bilaterally symmetric organisms, their internal organs are distributed asymmetrically along a left-right axis. Disruption of left-right axis asymmetric patterning often occurs in human genetic disorders. In zebrafish embryos, Kupffer’s vesicle, like the mouse node, breaks symmetry by inducing asymmetric expression of the Nodal-related gene, spaw, in the left lateral plate mesoderm (LPM). Spaw then stimulates transcription of itself and downstream genes, including lft1, lft2, and pitx2, specifically in the left side of the diencephalon, heart and LPM. This developmental step is essential to establish subsequent asymmetric organ positioning. In this study, we evaluated the role of krüppel-like factor 8 (klf8) in regulating left-right asymmetric patterning in zebrafish embryos. Methods Zebrafish klf8 expression was disrupted by both morpholino antisense oligomer-mediated knockdown and a CRISPR-Cas9 system. Whole-mount in situ hybridization was conducted to evaluate gene expression patterns of Nodal signalling components and the positions of heart and visceral organs. Dorsal forerunner cell number was evaluated in Tg(sox17:gfp) embryos and the length and number of cilia in Kupffer’s vesicle were analyzed by immunocytochemistry using an acetylated tubulin antibody. Results Heart jogging, looping and visceral organ positioning were all defective in zebrafish klf8 morphants. At the 18–22 s stages, klf8 morphants showed reduced expression of genes encoding Nodal signalling components (spaw, lft1, lft2, and pitx2) in the left LPM, diencephalon, and heart. Co-injection of klf8 mRNA with klf8 morpholino partially rescued spaw expression. Furthermore, klf8 but not klf8△zf overexpressing embryos showed dysregulated bilateral expression of Nodal signalling components at late somite stages. At the 10s stage, klf8 morphants exhibited reductions in length and number of cilia in Kupffer’s vesicle, while at 75% epiboly, fewer dorsal forerunner cells were observed. Interestingly, klf8 mutant embryos, generated by a CRISPR-Cas9 system, showed bilateral spaw expression in the LPM at late somite stages. This observation may be partly attributed to compensatory upregulation of klf12b, because klf12b knockdown reduced the percentage of klf8 mutants exhibiting bilateral spaw expression. Conclusions Our results demonstrate that zebrafish Klf8 regulates left-right asymmetric patterning by modulating both Kupffer’s vesicle morphogenesis and spaw expression in the left LPM.
- Published
- 2017
- Full Text
- View/download PDF
4. Fractionation and identification of 9c, 11t, 13t-conjugated linolenic acid as an activator of PPARα in bitter gourd (Momordica charantia L.)
- Author
-
Chuang, Chia-Ying, Hsu, Chin, Chao, Che-Yi, Wein, Yung-Shung, Kuo, Yueh-Hsiung, and Huang, Ching-jang
- Published
- 2006
- Full Text
- View/download PDF
5. Bitter gourd(Momordica charantia) extract activates peroxisome proliferator-activated receptors and upregulates the expression of the acyl CoA oxidase gene in H4IIEC3 hepatoma cells
- Author
-
Chao, Che-Yi and Huang, Ching-jang
- Published
- 2003
- Full Text
- View/download PDF
6. β-Lapachone induces heart morphogenetic and functional defects by promoting the death of erythrocytes and the endocardium in zebrafish embryos
- Author
-
Huang Chang-Jen, Lu Yu-Fen, Chen Yi-Hua, Tsai Ming-Yuan, Lin Che Yi, Wu Yi-Ting, Cheng Chao-Min, and Hwang Sheng-Ping L
- Subjects
zebrafish ,β-lapachone ,heart morphogenesis ,erythrocyte deficiency ,endocardium ,apoptosis ,Medicine - Abstract
Abstract Background β-Lapachone has antitumor and wound healing-promoting activities. To address the potential influences of various chemicals on heart development of zebrafish embryos, we previously treated zebrafish embryos with chemicals from a Sigma LOPAC1280™ library and found several chemicals including β-lapachone that affected heart morphogenesis. In this study, we further evaluated the effects of β-lapachone on zebrafish embryonic heart development. Methods Embryos were treated with β-lapachone or dimethyl sulfoxide (DMSO) at 24 or 48 hours post fertilization (hpf) for 4 h at 28°C. Heart looping and valve development was analyzed by whole-mount in situ hybridization and histological analysis. For fractional shortening and wall shear stress analyses, AB and Tg (gata1:DsRed) embryos were recorded for their heart pumping and blood cell circulations via time-lapse fluorescence microscopy. Dextran rhodamine dye injection into the tail reticular cells was used to analyze circulation. Reactive oxygen species (ROS) was analyzed by incubating embryos in 5-(and 6-)-chloromethyl-2',7'-dichloro-dihydrofluorescein diacetate (CM-H2DCFDA) and recorded using fluorescence microscopy. o-Dianisidine (ODA) staining and whole mount in situ hybridization were used to analyze erythrocytes. TUNEL assay was used to examine DNA fragmentation. Results We observed a linear arrangement of the ventricle and atrium, bradycardia arrhythmia, reduced fractional shortening, circulation with a few or no erythrocytes, and pericardial edema in β-lapachone-treated 52-hpf embryos. Abnormal expression patterns of cmlc2, nppa, BMP4, versican, and nfatc1, and histological analyses showed defects in heart-looping and valve development of β-lapachone-treated embryos. ROS production was observed in erythrocytes and DNA fragmentation was detected in both erythrocytes and endocardium of β-lapachone-treated embryos. Reduction in wall shear stress was uncovered in β-lapachone-treated embryos. Co-treatment with the NQO1 inhibitor, dicoumarol, or the calcium chelator, BAPTA-AM, rescued the erythrocyte-deficiency in circulation and heart-looping defect phenotypes in β-lapachone-treated embryos. These results suggest that the induction of apoptosis of endocardium and erythrocytes by β-lapachone is mediated through an NQO1- and calcium-dependent pathway. Conclusions The novel finding of this study is that β-lapachone affects heart morphogenesis and function through the induction of apoptosis of endocardium and erythrocytes. In addition, this study further demonstrates the importance of endocardium and hemodynamic forces on heart morphogenesis and contractile performance.
- Published
- 2011
- Full Text
- View/download PDF
7. Klf8 regulates left-right asymmetric patterning through modulation of Kupffer’s vesicle morphogenesis and spaw expression
- Author
-
Sheng-Ping L. Hwang, Huang-Wei Lien, Ming-Yuan Tsai, Yu-Fen Lu, Hsin-Chi Liao, Yu-Hsiu Liu, Yun-Ren Lai, Chang-Jen Huang, Yi Chung Chen, Che-Yi Lin, and Chung-Hsiang Yang
- Subjects
0301 basic medicine ,animal structures ,Morpholino ,Spaw ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Kruppel-Like Transcription Factors ,lcsh:Medicine ,Epiboly ,Biology ,Transforming Growth Factor beta2 ,03 medical and health sciences ,Morphogenesis ,medicine ,Animals ,Pharmacology (medical) ,Molecular Biology ,Zebrafish ,Body Patterning ,Gene knockdown ,Research ,Lateral plate mesoderm ,lcsh:R ,Biochemistry (medical) ,L-R patterning ,Gene Expression Regulation, Developmental ,Klf8 ,Cell Biology ,General Medicine ,Anatomy ,Zebrafish Proteins ,biology.organism_classification ,Cell biology ,Somite ,030104 developmental biology ,medicine.anatomical_structure ,Kupffer’s vesicle ,embryonic structures ,Heart jogging ,NODAL - Abstract
Background Although vertebrates are bilaterally symmetric organisms, their internal organs are distributed asymmetrically along a left-right axis. Disruption of left-right axis asymmetric patterning often occurs in human genetic disorders. In zebrafish embryos, Kupffer’s vesicle, like the mouse node, breaks symmetry by inducing asymmetric expression of the Nodal-related gene, spaw, in the left lateral plate mesoderm (LPM). Spaw then stimulates transcription of itself and downstream genes, including lft1, lft2, and pitx2, specifically in the left side of the diencephalon, heart and LPM. This developmental step is essential to establish subsequent asymmetric organ positioning. In this study, we evaluated the role of krüppel-like factor 8 (klf8) in regulating left-right asymmetric patterning in zebrafish embryos. Methods Zebrafish klf8 expression was disrupted by both morpholino antisense oligomer-mediated knockdown and a CRISPR-Cas9 system. Whole-mount in situ hybridization was conducted to evaluate gene expression patterns of Nodal signalling components and the positions of heart and visceral organs. Dorsal forerunner cell number was evaluated in Tg(sox17:gfp) embryos and the length and number of cilia in Kupffer’s vesicle were analyzed by immunocytochemistry using an acetylated tubulin antibody. Results Heart jogging, looping and visceral organ positioning were all defective in zebrafish klf8 morphants. At the 18–22 s stages, klf8 morphants showed reduced expression of genes encoding Nodal signalling components (spaw, lft1, lft2, and pitx2) in the left LPM, diencephalon, and heart. Co-injection of klf8 mRNA with klf8 morpholino partially rescued spaw expression. Furthermore, klf8 but not klf8△zf overexpressing embryos showed dysregulated bilateral expression of Nodal signalling components at late somite stages. At the 10s stage, klf8 morphants exhibited reductions in length and number of cilia in Kupffer’s vesicle, while at 75% epiboly, fewer dorsal forerunner cells were observed. Interestingly, klf8 mutant embryos, generated by a CRISPR-Cas9 system, showed bilateral spaw expression in the LPM at late somite stages. This observation may be partly attributed to compensatory upregulation of klf12b, because klf12b knockdown reduced the percentage of klf8 mutants exhibiting bilateral spaw expression. Conclusions Our results demonstrate that zebrafish Klf8 regulates left-right asymmetric patterning by modulating both Kupffer’s vesicle morphogenesis and spaw expression in the left LPM. Electronic supplementary material The online version of this article (doi:10.1186/s12929-017-0351-y) contains supplementary material, which is available to authorized users.
- Published
- 2017
8. Klf8 regulates left-right asymmetric patterning through modulation of Kupffer’s vesicle morphogenesis and spaw expression
- Author
-
Lin, Che-Yi, primary, Tsai, Ming-Yuan, additional, Liu, Yu-Hsiu, additional, Lu, Yu-Fen, additional, Chen, Yi-Chung, additional, Lai, Yun-Ren, additional, Liao, Hsin-Chi, additional, Lien, Huang-Wei, additional, Yang, Chung-Hsiang, additional, Huang, Chang-Jen, additional, and Hwang, Sheng-Ping L., additional
- Published
- 2017
- Full Text
- View/download PDF
9. Bitter gourd(Momordica charantia) extract activates peroxisome proliferator-activated receptors and upregulates the expression of the acyl CoA oxidase gene in H4IIEC3 hepatoma cells
- Author
-
Che-Yi Chao and Ching-jang Huang
- Subjects
Endocrinology, Diabetes and Metabolism ,Biochemistry (medical) ,Clinical Biochemistry ,Pharmacology (medical) ,Cell Biology ,General Medicine ,Molecular Biology - Published
- 2003
10. Subject Index Vol. 10, 2003
- Author
-
Mei-Sue Chen, Jen-Hwey Chiu, Hsing I. Chen, Wann-Cherng Perng, Jianning Wei, Chien-Hung Chen, Ya-Chen Liu, Małgorzata Szereda-Przestaszewska, Hong-Jen Lee, Sumio Sugano, Shu-Min Lin, Ann-Ping Tsou, Stephen C. Fowler, Chu-Wen Yang, Annelies Hauspie, Nada H. Khattar, Jen-Chine Wu, Wei-Kuang Liu, Richard B. Markham, David Camerini, Rong Chen, Christine Neuveut, Yi-Da Chung, Seng-Sheen Fan, Chien-Wen Hou, Chien-Huang Lin, Meng-Chun Hu, Carl Denef, Chin-Pyng Wu, Chien-Ying Liu, Marcin Rozalski, Ing-Cherng Guo, Yi-Ting Chen, Chen-Kung Chou, Y.S. Chan, Wei-Teing Chen, Luo-Hwa Miau, Jin-Tun Lin, Chain Fa Su, Chia-Hua Kuo, Laura De Marchis, Mei-Ling Chang, Chih-Ten Yu, Cezary Watala, Yu-Lun Liao, Eve Seuntjens, Vivian C. Yang, Di Sha, Wen-Hsin Huang, Horng-Chyuan Lin, Chun-Chung Lee, D.K.Y. Shum, Yu-Chi Chuang, Jung-Yaw Lin, Wan-An Lu, Jacek Golanski, Ben Berkhout, Cheng-Deng Kuo, Hsin-Yi Ho, Kerry Wu, Vincent J. Blanch, Wen-Chang Chang, Jang-Yen Wu, Chun-Hua Wang, Daniel Cupac, Kou-Gi Shyu, David Wang, Wen-Hsin Chang, Han-Pin Kuo, Ching-Hung Lin, Che-Yi Chao, Sharon Bargo, Chia-Chu Tsai, Jui-Fen Lin, K.K.L. Yung, Ru Ping Lee, Michael M.C. Lai, Beata Kopczyńska, June L. Traicoff, Wei-Ting Chao, Yutaka Suzuku, Charlotte S. Kaetzel, Kuan-Teh Jeang, Ying Jin, Kun-Ze Lee, Ying-Chih Chi, Robert M. Scoggins, Shankung Lin, Bao-Wei Wang, Shang Jyh Kao, Rodolfo E. Zamora, Britten L. Ginsburg, I-Jung Lu, Heng Wu, Ding-Shinn Chen, Bon Chu Chung, Hang Chang, Boguslawa Luzak, Yu-Ling Sung, Albert M. Wu, Wen-Chih Lee, C.H. Lai, Dennis J. Templeton, Yu-Chia Su, P.C. Joost Haasnoot, Jin-Yuan Su, Hugo Vankelecom, Daniel Fu-Chang Tsai, Fu-Chiu Yu, L.W. Chen, John T. Kung, Ling-Ling Chiou, Hsuan-Shu Lee, F.X. Zhang, Sarah J. Plummer, Guan-Tarn Huang, Pei-Ming Yang, Shih-Wei Chou, Horng-Chin Yan, Li-Chi Ku, Yun-Hen Liu, Samuel H.H. Chan, Ji-Chuu Hwang, Jin-Chuan Sheu, Ching-jang Huang, Shiow-Chwen Tsai, and Graham Casey
- Subjects
Index (economics) ,Endocrinology, Diabetes and Metabolism ,Biochemistry (medical) ,Clinical Biochemistry ,Statistics ,Pharmacology (medical) ,Subject (documents) ,Cell Biology ,General Medicine ,Molecular Biology ,Mathematics - Published
- 2003
11. Contents Vol. 10, 2003
- Author
-
Jin-Chuan Sheu, Hong-Jen Lee, Ching-jang Huang, Chien-Hung Chen, Fu-Chiu Yu, Shiow-Chwen Tsai, Pei-Ming Yang, Li-Chi Ku, Chia-Hua Kuo, Graham Casey, Ji-Chuu Hwang, Ya-Chen Liu, Seng-Sheen Fan, Chien-Wen Hou, Rodolfo E. Zamora, Y.S. Chan, Sarah J. Plummer, Jen-Chine Wu, Chien-Ying Liu, Bon Chu Chung, Mei-Sue Chen, Chen-Kung Chou, Horng-Chyuan Lin, Guan-Tarn Huang, Hsing I. Chen, Wei-Teing Chen, Laura De Marchis, F.X. Zhang, Cezary Watala, Jung-Yaw Lin, Yi-Ting Chen, D.K.Y. Shum, Nada H. Khattar, Kerry Wu, Mei-Ling Chang, Charlotte S. Kaetzel, Che-Yi Chao, Ing-Cherng Guo, Chin-Pyng Wu, Vincent J. Blanch, Beata Kopczyńska, Ben Berkhout, Yu-Lun Liao, Jui-Fen Lin, Wen-Hsin Huang, Cheng-Deng Kuo, Daniel Cupac, K.K.L. Yung, David Wang, Han-Pin Kuo, Wei-Ting Chao, Yutaka Suzuku, Yu-Chia Su, Chun-Hua Wang, Kun-Ze Lee, Ying-Chih Chi, Yu-Chi Chuang, P.C. Joost Haasnoot, I-Jung Lu, Albert M. Wu, Ding-Shinn Chen, Dennis J. Templeton, Ching-Hung Lin, Wen-Chih Lee, Jin-Yuan Su, C.H. Lai, Hugo Vankelecom, Britten L. Ginsburg, Wen-Hsin Chang, Heng Wu, Bao-Wei Wang, Shang Jyh Kao, Wan-An Lu, Jin-Tun Lin, Daniel Fu-Chang Tsai, Wei-Kuang Liu, Hang Chang, Boguslawa Luzak, Chih-Ten Yu, Hsin-Yi Ho, Yu-Ling Sung, Shu-Min Lin, Sharon Bargo, Wen-Chang Chang, Annelies Hauspie, Michael M.C. Lai, L.W. Chen, Yi-Da Chung, John T. Kung, Ling-Ling Chiou, Hsuan-Shu Lee, Jianning Wei, Chu-Wen Yang, David Camerini, June L. Traicoff, Marcin Rozalski, Vivian C. Yang, Jacek Golanski, Di Sha, Małgorzata Szereda-Przestaszewska, Robert M. Scoggins, Shankung Lin, Ru Ping Lee, Rong Chen, Yun-Hen Liu, Meng-Chun Hu, Samuel H.H. Chan, Ann-Ping Tsou, Stephen C. Fowler, Richard B. Markham, Shih-Wei Chou, Carl Denef, Jen-Hwey Chiu, Kuan-Teh Jeang, Chien-Huang Lin, Ying Jin, Horng-Chin Yan, Chain Fa Su, Eve Seuntjens, Sumio Sugano, Chun-Chung Lee, Wann-Cherng Perng, Christine Neuveut, Kou-Gi Shyu, Chia-Chu Tsai, Jang-Yen Wu, and Luo-Hwa Miau
- Subjects
Endocrinology, Diabetes and Metabolism ,Biochemistry (medical) ,Clinical Biochemistry ,Pharmacology (medical) ,Cell Biology ,General Medicine ,Molecular Biology - Published
- 2003
12. β-Lapachone induces heart morphogenetic and functional defects by promoting the death of erythrocytes and the endocardium in zebrafish embryos
- Author
-
Ming-Yuan Tsai, Chao-Min Cheng, Yu-Fen Lu, Sheng-Ping L. Hwang, Yi-Hua Chen, Che Yi Lin, Yi-Ting Wu, and Chang-Jen Huang
- Subjects
Heart Defects, Congenital ,Dicumarol ,Heart morphogenesis ,Erythrocytes ,animal structures ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Embryonic Development ,lcsh:Medicine ,In situ hybridization ,Time-Lapse Imaging ,heart morphogenesis ,Morphogenesis ,NAD(P)H Dehydrogenase (Quinone) ,Animals ,Dimethyl Sulfoxide ,Pharmacology (medical) ,Heart looping ,Molecular Biology ,Zebrafish ,Endocardium ,Biochemistry, medical ,biology ,Heart development ,Embryonic heart ,Research ,lcsh:R ,Biochemistry (medical) ,β-lapachone ,apoptosis ,Gene Expression Regulation, Developmental ,Heart ,erythrocyte deficiency ,Cell Biology ,General Medicine ,zebrafish ,biology.organism_classification ,Cell biology ,Microscopy, Fluorescence ,endocardium ,embryonic structures ,Erythrocyte Count ,DNA fragmentation ,Reactive Oxygen Species ,Naphthoquinones - Abstract
Background β-Lapachone has antitumor and wound healing-promoting activities. To address the potential influences of various chemicals on heart development of zebrafish embryos, we previously treated zebrafish embryos with chemicals from a Sigma LOPAC1280™ library and found several chemicals including β-lapachone that affected heart morphogenesis. In this study, we further evaluated the effects of β-lapachone on zebrafish embryonic heart development. Methods Embryos were treated with β-lapachone or dimethyl sulfoxide (DMSO) at 24 or 48 hours post fertilization (hpf) for 4 h at 28°C. Heart looping and valve development was analyzed by whole-mount in situ hybridization and histological analysis. For fractional shortening and wall shear stress analyses, AB and Tg (gata1:DsRed) embryos were recorded for their heart pumping and blood cell circulations via time-lapse fluorescence microscopy. Dextran rhodamine dye injection into the tail reticular cells was used to analyze circulation. Reactive oxygen species (ROS) was analyzed by incubating embryos in 5-(and 6-)-chloromethyl-2',7'-dichloro-dihydrofluorescein diacetate (CM-H2DCFDA) and recorded using fluorescence microscopy. o-Dianisidine (ODA) staining and whole mount in situ hybridization were used to analyze erythrocytes. TUNEL assay was used to examine DNA fragmentation. Results We observed a linear arrangement of the ventricle and atrium, bradycardia arrhythmia, reduced fractional shortening, circulation with a few or no erythrocytes, and pericardial edema in β-lapachone-treated 52-hpf embryos. Abnormal expression patterns of cmlc2, nppa, BMP4, versican, and nfatc1, and histological analyses showed defects in heart-looping and valve development of β-lapachone-treated embryos. ROS production was observed in erythrocytes and DNA fragmentation was detected in both erythrocytes and endocardium of β-lapachone-treated embryos. Reduction in wall shear stress was uncovered in β-lapachone-treated embryos. Co-treatment with the NQO1 inhibitor, dicoumarol, or the calcium chelator, BAPTA-AM, rescued the erythrocyte-deficiency in circulation and heart-looping defect phenotypes in β-lapachone-treated embryos. These results suggest that the induction of apoptosis of endocardium and erythrocytes by β-lapachone is mediated through an NQO1- and calcium-dependent pathway. Conclusions The novel finding of this study is that β-lapachone affects heart morphogenesis and function through the induction of apoptosis of endocardium and erythrocytes. In addition, this study further demonstrates the importance of endocardium and hemodynamic forces on heart morphogenesis and contractile performance.
- Published
- 2011
13. Fractionation and identification of 9c, 11t, 13t-conjugated linolenic acid as an activator of PPARalpha in bitter gourd (Momordica charantia L.)
- Author
-
Yung-Shung Wein, Yueh-Hsiung Kuo, Chia-Ying Chuang, Che-Yi Chao, Ching-jang Huang, and Chin Hsu
- Subjects
Momordica charantia ,Linolenic acid ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Bitter gourd ,CHO Cells ,Cricetulus ,Cricetinae ,Glucose homeostasis ,Acyl-CoA oxidase ,Animals ,Pharmacology (medical) ,PPAR alpha ,Receptor ,Molecular Biology ,Momordica ,biology ,Activator (genetics) ,Biochemistry (medical) ,alpha-Linolenic Acid ,Cell Biology ,General Medicine ,Peroxisome ,biology.organism_classification ,Biochemistry ,Spectrophotometry, Ultraviolet - Abstract
Bitter gourd (Momordica charantia L.) is a common vegetable in Asia that has been used in traditional medicine for the treatment of Diabetes. PPARs are ligand-dependent transcription factors that belong to the steroid hormone nuclear receptor family and control lipid and glucose homeostasis in the body. We previously reported that the ethyl acetate (EA) extract of bitter gourd activated peroxisome proliferator receptors (PPARs) alpha and gamma. To identify the active compound that activated PPARalpha, wild bitter gourd EA extract was partitioned between n-hexane and 90% methanol/10% H(2)O, and the n-hexane soluble fraction was further separated by silica gel column chromatography and finally by preparative HPLC. A transactivation assay employing a clone of CHOK1 cells stably transfected with a (UAS)(4)-tk-alkaline phosphatase reporter and a chimeric receptor of GAL4-rPPARalpha LBD was used to track the active component. Based on Mass, NMR, and IR spectroscopy, 9cis, 11trans, 13trans-conjugated linolenic acid (9c, 11t, 13t-CLN) was identified as a PPARalpha activator in wild bitter gourd. The isolated 9c, 11t, 13t-CLN rich fraction also significantly induced acyl CoA oxidase (ACO) activity in a peroxisome proliferator-responsive murine hepatoma cell line, H4IIEC3, implying that 9c, 11t, 13t-CLN was able to act on a natural PPARalpha signaling pathway as well. The content of 9c, 11t, 13t-CLN was estimated to be about 7.1 g/kg of our dried wild bitter gourd sample. The concentration of 9c, 11t, 13t-CLN and activation activity in the hydrolyzed EA extract of the seeds was higher than that of the flesh. The potential health benefits of 9c, 11t, 13t-CLN through the PPARalpha regulated mechanism are worthy to be further characterized in in vivo studies.
- Published
- 2006
14. Bitter gourd (Momordica charantia) extract activates peroxisome proliferator-activated receptors and upregulates the expression of the acyl CoA oxidase gene in H4IIEC3 hepatoma cells
- Author
-
Che-Yi Chao and Ching-jang Huang
- Subjects
Transcriptional Activation ,Momordica charantia ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Bitter gourd ,Receptors, Cytoplasmic and Nuclear ,Transfection ,Transactivation ,Mice ,Genes, Reporter ,Cell Line, Tumor ,Acyl-CoA oxidase ,Animals ,Pharmacology (medical) ,Receptor ,Molecular Biology ,Analysis of Variance ,Momordica ,biology ,Chemistry ,Plant Extracts ,Biochemistry (medical) ,food and beverages ,Cell Biology ,General Medicine ,Peroxisome ,biology.organism_classification ,Blotting, Northern ,Biochemistry ,Gene Expression Regulation ,Peroxisome proliferator-activated receptor alpha ,Acyl-CoA Oxidase ,Signal transduction ,Signal Transduction ,Transcription Factors - Abstract
Peroxisome proliferator-activated receptor alpha (PPARalpha) is a ligand-dependent transcription factor that regulates the expression of genes involved in lipid metabolism and transport. Ligands/activators of PPARalpha, like fibrate-type drugs, may have hypolipidemic effects. To identify food that contains activators of PPARalpha, a transactivation assay employing a clone of CHO-K1 cells stably transfected with a (UAS)(4)-tk-alkaline phosphatase reporter and a chimeric receptor of Gal4-rPPARalpha LBD was used to screen ethyl acetate (EA) extracts of a large variety of food materials. It was found that the EA extract of bitter gourd (Momordica charantia), a common oriental vegetable, activated PPARalpha to an extent that was equivalent to or even higher than 10 microM Wy-14643, a known ligand of PPARalpha. This extract also activated PPARgamma to a significant extent which was comparable to 0.5 microM BRL-49653. The activity toward PPARalpha was mainly in the soluble fraction of the organic solvent. The EA extract prepared from the whole fruit showed significantly higher activity than that from seeds or flesh alone. The bitter gourd EA extract was then incorporated into the medium for treatment of a peroxisome proliferator-responsive murine hepatoma cell line, H4IIEC3, for 72 h. Treated cells showed significantly higher activity of acyl CoA oxidase and higher expressions of mRNA of this enzyme and fatty acid-binding protein, indicating that the bitter gourd EA extract was able to act on a natural PPARalpha signaling pathway in this cell line. It is thus worth further investigating the PPAR-associated health benefits of bitter gourd.
- Published
- 2003
15. β-Lapachone induces heart morphogenetic and functional defects by promoting the death of erythrocytes and the endocardium in zebrafish embryos
- Author
-
Wu, Yi-Ting, primary, Lin, Che Yi, additional, Tsai, Ming-Yuan, additional, Chen, Yi-Hua, additional, Lu, Yu-Fen, additional, Huang, Chang-Jen, additional, Cheng, Chao-Min, additional, and Hwang, Sheng-Ping L, additional
- Published
- 2011
- Full Text
- View/download PDF
16. Bitter Gourd (Momordica charantia) Extract Activates Peroxisome Proliferator-Activated Receptors and Upregulates the Expression of the Acyl CoA Oxidase Gene in H4IIEC3 Hepatoma Cells
- Author
-
Chao, Che-Yi, primary and Huang, Ching-jang, additional
- Published
- 2003
- Full Text
- View/download PDF
17. Fractionation and identification of 9 c, 11 t, 13 t-conjugated linolenic acid as an activator of PPARα in bitter gourd ( Momordica charantia L.).
- Author
-
Chuang, Chia-Ying, Hsu, Chin, Chao, Che-Yi, Wein, Yung-Shung, Kuo, Yueh-Hsiung, and Huang, Ching-jang
- Subjects
MOMORDICA charantia ,PEROXISOMES ,TRADITIONAL medicine ,TREATMENT of diabetes ,STEROID receptors ,LIGANDS (Biochemistry) ,TRANSCRIPTION factors ,HOMEOSTASIS ,CHROMATOGRAPHIC analysis - Abstract
Bitter gourd ( Momordica charantia L.) is a common vegetable in Asia that has been used in traditional medicine for the treatment of Diabetes. PPARs are ligand-dependent transcription factors that belong to the steroid hormone nuclear receptor family and control lipid and glucose homeostasis in the body. We previously reported that the ethyl acetate (EA) extract of bitter gourd activated peroxisome proliferator receptors (PPARs) α and γ. To identify the active compound that activated PPARα, wild bitter gourd EA extract was partitioned between n-hexane and 90% methanol/10% H
2 O, and the n-hexane soluble fraction was further separated by silica gel column chromatography and finally by preparative HPLC. A transactivation assay employing a clone of CHOK1 cells stably transfected with a (UAS)4 -tk-alkaline phosphatase reporter and a chimeric receptor of GAL4-rPPARα LBD was used to track the active component. Based on Mass, NMR, and IR spectroscopy, 9 cis, 11 trans, 13 trans-conjugated linolenic acid (9 c, 11 t, 13 t-CLN) was identified as a PPARα activator in wild bitter gourd. The isolated 9 c, 11 t, 13 t-CLN rich fraction also significantly induced acyl CoA oxidase (ACO) activity in a peroxisome proliferator-responsive murine hepatoma cell line, H4IIEC3, implying that 9 c, 11 t, 13 t-CLN was able to act on a natural PPARα signaling pathway as well. The content of 9 c, 11 t, 13 t-CLN was estimated to be about 7.1 g/kg of our dried wild bitter gourd sample. The concentration of 9 c, 11 t, 13 t-CLN and activation activity in the hydrolyzed EA extract of the seeds was higher than that of the flesh. The potential health benefits of 9 c, 11 t, 13 t-CLN through the PPARα regulated mechanism are worthy to be further characterized in in vivo studies. [ABSTRACT FROM AUTHOR]- Published
- 2006
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.