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1. Exogenous MG53 Protects Adult Mouse Cardiomyocytes by Preventing Mitochondrial Damage in Response to Oxidative Stress

Author

Gumpper, Kristyn, Xinyu Zhou, Park, Ki Ho, Renzhi Han, Pei-Hui Lin, and Jianjie Ma

Subjects
Physiology, FOS: Biological sciences, Cardiology, 60802 Animal Cell and Molecular Biology, Cell Biology, 60602 Animal Physiology - Cell
Abstract

Ischemic heart disease is a major cause of mortality and morbidity world-wide and its incidence is continually increasing as other health factors, such as diabetes type II and obesity, climb. Ischemic injury of any tissue causes a loss of healthy mitochondria, due to an increase in reactive oxygen species leading to oxidative stress. MG53, also known as TRIM72, is highly expressed in skeletal muscle and modestly in other tissues and is essential to repair damage to plasma membrane by acting as a myokine. We have previously shown that MG53’s membrane repair function is associated with changes in oxidative state inside the cell. Moreover, we have shown that mg53−/− mice are more susceptible to ischemia-reperfusion injury, whereas treatment with exogenous recombinant human MG53 (rhMG53) reduces both infarct damage and fibrosis and restores cardiac function. We hypothesize that in addition to cell membrane repair, exogenous MG53 enters cardiomyocytes and can act as a myokine to protect cardiomyocytes by maintaining mitochondrial function through control of oxidative-stress induced mitophagy. In this study, MG53 protection of cardiomyocyte mitochondria was assessed by subjecting HL-1 cells (an immortalized mouse atrial cardiomyocyte cell line) to oxidative stress followed by analysis for mitochondrial structure and function. Overall, we show that treatment with rhMG53 allowed cells to maintain a healthy mitochondrial membrane potential to protect mitochondrial function. We are currently dissecting the mechanism that facilitates the endocytic uptake of MG53 from the circulation into the cardiomyocytes as well as downstream signaling pathways that mediate the protection of the mitochondria function. The novelty of this study is that it shows exogenous MG53 can protect mitochondria in cardiomyocytes upon oxidative stress. This provides a mechanism behind how rhMG53 treatment may be a clinically relevant strategy to reduce cardiomyocyte injury and maintain cardiac function in patients after ischemic injuries.

Published
2019
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2. Genetic association study of exfoliation syndrome identifies a protective rare variant at LOXL1 and five new susceptibility loci

Author

Aung, Tin, Ozaki, Mineo, Lee, Mei Chin, Schlötzer-Schrehardt, Ursula, Thorleifsson, Gudmar, Mizoguchi, Takanori, Igo, Robert P, Haripriya, Aravind, Williams, Susan E, Astakhov, Yury S, Orr, Andrew C, Burdon, Kathryn P, Nakano, Satoko, Mori, Kazuhiko, Abu-Amero, Khaled, Hauser, Michael, Li, Zheng, Prakadeeswari, Gopalakrishnan, Bailey, Jessica N Cooke, Cherecheanu, Alina Popa, Kang, Jae H, Nelson, Sarah, Hayashi, Ken, Manabe, Shin-Ichi, Kazama, Shigeyasu, Zarnowski, Tomasz, Inoue, Kenji, Irkec, Murat, Coca-Prados, Miguel, Sugiyama, Kazuhisa, Järvelä, Irma, Schlottmann, Patricio, Lerner, S Fabian, Lamari, Hasnaa, Nilgün, Yildirim, Bikbov, Mukharram, Park, Ki Ho, Cha, Soon Cheol, Yamashiro, Kenji, Zenteno, Juan C, Jonas, Jost B, Kumar, Rajesh S, Perera, Shamira A, Chan, Anita SY, Kobakhidze, Nino, George, Ronnie, Vijaya, Lingam, Do, Tan, Edward, Deepak P, de Juan Marcos, Lourdes, Pakravan, Mohammad, Moghimi, Sasan, Ideta, Ryuichi, Bach-Holm, Daniella, Kappelgaard, Per, Wirostko, Barbara, Thomas, Samuel, Gaston, Daniel, Bedard, Karen, Greer, Wenda L, Yang, Zhenglin, Chen, Xueyi, Huang, Lulin, Sang, Jinghong, Jia, Hongyan, Jia, Liyun, Qiao, Chunyan, Zhang, Hui, Liu, Xuyang, Zhao, Bowen, Wang, Ya-Xing, Xu, Liang, Leruez, Stéphanie, Reynier, Pascal, Chichua, George, Tabagari, Sergo, Uebe, Steffen, Zenkel, Matthias, Berner, Daniel, Mossböck, Georg, Weisschuh, Nicole, Hoja, Ursula, Welge-Luessen, Ulrich-Christoph, Mardin, Christian, Founti, Panayiota, Chatzikyriakidou, Anthi, Pappas, Theofanis, Anastasopoulos, Eleftherios, Lambropoulos, Alexandros, Ghosh, Arkasubhra, Shetty, Rohit, Porporato, Natalia, Saravanan, Vijayan, Venkatesh, Rengaraj, Shivkumar, Chandrashekaran, Kalpana, Narendran, Sarangapani, Sripriya, Kanavi, Mozhgan R, Beni, Afsaneh Naderi, and Yazdani, Shahin

Subjects
Asian Continental Ancestry Group, Male, Messenger, and over, Eye, Exfoliation Syndrome, Medical and Health Sciences, Rare Diseases, Asian People, Cell Adhesion, 80 and over, Genetics, Humans, Point Mutation, 2.1 Biological and endogenous factors, Genetic Predisposition to Disease, Aetiology, Alleles, Aged, Gene Expression Profiling, Prevention, Human Genome, Biological Sciences, eye diseases, Extracellular Matrix, Amino Acid Substitution, Haplotypes, Mutation, RNA, Female, Cellular, Amino Acid Oxidoreductases, Calcium Channels, Spheroids, Missense, Molecular Chaperones, Genome-Wide Association Study, Developmental Biology
Abstract

Exfoliation syndrome (XFS) is the most common known risk factor for secondary glaucoma and a major cause of blindness worldwide. Variants in two genes, LOXL1 and CACNA1A, have previously been associated with XFS. To further elucidate the genetic basis of XFS, we collected a global sample of XFS cases to refine the association at LOXL1, which previously showed inconsistent results across populations, and to identify new variants associated with XFS. We identified a rare protective allele at LOXL1 (p.Phe407, odds ratio (OR) = 25, P = 2.9 × 10-14) through deep resequencing of XFS cases and controls from nine countries. A genome-wide association study (GWAS) of XFS cases and controls from 24 countries followed by replication in 18 countries identified seven genome-wide significant loci (P < 5 × 10-8). We identified association signals at 13q12 (POMP), 11q23.3 (TMEM136), 6p21 (AGPAT1), 3p24 (RBMS3) and 5q23 (near SEMA6A). These findings provide biological insights into the pathology of XFS and highlight a potential role for naturally occurring rare LOXL1 variants in disease biology.

Published
2017

3. Genome-wide association study identifies five new susceptibility loci for primary angle closure glaucoma

Author

Khor, Chiea Chuen, Do, Tan, Jia, Hongyan, Nakano, Masakazu, George, Ronnie, Abu-Amero, Khaled, Duvesh, Roopam, Chen, Li Jia, Li, Zheng, Nongpiur, Monisha E, Perera, Shamira A, Qiao, Chunyan, Wong, Hon-Tym, Sakai, Hiroshi, Barbosa de Melo, Mônica, Lee, Mei-Chin, Chan, Anita S, Azhany, Yaakub, Dao, Thi Lam Huong, Ikeda, Yoko, Perez-Grossmann, Rodolfo A, Zarnowski, Tomasz, Day, Alexander C, Jonas, Jost B, Tam, Pancy OS, Tran, Tuan Anh, Ayub, Humaira, Akhtar, Farah, Micheal, Shazia, Chew, Paul TK, Aljasim, Leyla A, Dada, Tanuj, Luu, Tam Thi, Awadalla, Mona S, Kitnarong, Naris, Wanichwecharungruang, Boonsong, Aung, Yee Yee, Mohamed-Noor, Jelinar, Vijayan, Saravanan, Sarangapani, Sripriya, Husain, Rahat, Jap, Aliza, Baskaran, Mani, Goh, David, Su, Daniel H, Wang, Huaizhou, Yong, Vernon K, Yip, Leonard W, Trinh, Tuyet Bach, Makornwattana, Manchima, Nguyen, Thanh Thu, Leuenberger, Edgar U, Park, Ki-Ho, Wiyogo, Widya Artini, Kumar, Rajesh S, Tello, Celso, Kurimoto, Yasuo, Thapa, Suman S, Pathanapitoon, Kessara, Salmon, John F, Sohn, Yong Ho, Fea, Antonio, Ozaki, Mineo, Lai, Jimmy SM, Tantisevi, Visanee, Khaing, Chaw Chaw, Mizoguchi, Takanori, Nakano, Satoko, Kim, Chan-Yun, Tang, Guangxian, Fan, Sujie, Wu, Renyi, Meng, Hailin, Nguyen, Thi Thuy Giang, Tran, Tien Dat, Ueno, Morio, Martinez, Jose Maria, Ramli, Norlina, Aung, Yin Mon, Reyes, Rigo Daniel, Vernon, Stephen A, Fang, Seng Kheong, Xie, Zhicheng, Chen, Xiao Yin, Foo, Jia Nee, Sim, Kar Seng, Wong, Tina T, Quek, Desmond T, Venkatesh, Rengaraj, Kavitha, Srinivasan, Krishnadas, Subbiah R, Soumittra, Nagaswamy, Shantha, Balekudaru, Lim, Boon-Ang, Ogle, Jeanne, de Vasconcellos, José PC, Costa, Vital P, Abe, Ricardo Y, de Souza, Bruno B, and Sng, Chelvin C

Subjects
Male, Genotype, Chromosome Mapping, Gene Expression, Glaucoma, Biological Sciences, Medical and Health Sciences, Cell Line, Angle-Closure, Genetic Loci, Humans, Genetic Predisposition to Disease, Female, Genome-Wide Association Study, Developmental Biology
Abstract

Primary angle closure glaucoma (PACG) is a major cause of blindness worldwide. We conducted a genome-wide association study (GWAS) followed by replication in a combined total of 10,503 PACG cases and 29,567 controls drawn from 24 countries across Asia, Australia, Europe, North America, and South America. We observed significant evidence of disease association at five new genetic loci upon meta-analysis of all patient collections. These loci are at EPDR1 rs3816415 (odds ratio (OR) = 1.24, P = 5.94 × 10(-15)), CHAT rs1258267 (OR = 1.22, P = 2.85 × 10(-16)), GLIS3 rs736893 (OR = 1.18, P = 1.43 × 10(-14)), FERMT2 rs7494379 (OR = 1.14, P = 3.43 × 10(-11)), and DPM2-FAM102A rs3739821 (OR = 1.15, P = 8.32 × 10(-12)). We also confirmed significant association at three previously described loci (P < 5 × 10(-8) for each sentinel SNP at PLEKHA7, COL11A1, and PCMTD1-ST18), providing new insights into the biology of PACG.

Published
2016

4. Genome-wide association study identifies five new susceptibility loci for primary angle closure glaucoma

Author

Khor, Chiea Chuen, Do, Tan, Jia, Hongyan, Nakano, Masakazu, George, Ronnie, Abu-Amero, Khaled, Duvesh, Roopam, Chen, Li Jia, Li, Zheng, Nongpiur, Monisha E, Perera, Shamira A, Qiao, Chunyan, Wong, Hon-Tym, Sakai, Hiroshi, Barbosa de Melo, Mônica, Lee, Mei-Chin, Chan, Anita S, Azhany, Yaakub, Dao, Thi Lam Huong, Ikeda, Yoko, Perez-Grossmann, Rodolfo A, Zarnowski, Tomasz, Day, Alexander C, Jonas, Jost B, Tam, Pancy OS, Tran, Tuan Anh, Ayub, Humaira, Akhtar, Farah, Micheal, Shazia, Chew, Paul TK, Aljasim, Leyla A, Dada, Tanuj, Luu, Tam Thi, Awadalla, Mona S, Kitnarong, Naris, Wanichwecharungruang, Boonsong, Aung, Yee Yee, Mohamed-Noor, Jelinar, Vijayan, Saravanan, Sarangapani, Sripriya, Husain, Rahat, Jap, Aliza, Baskaran, Mani, Goh, David, Su, Daniel H, Wang, Huaizhou, Yong, Vernon K, Yip, Leonard W, Trinh, Tuyet Bach, Makornwattana, Manchima, Nguyen, Thanh Thu, Leuenberger, Edgar U, Park, Ki-Ho, Wiyogo, Widya Artini, Kumar, Rajesh S, Tello, Celso, Kurimoto, Yasuo, Thapa, Suman S, Pathanapitoon, Kessara, Salmon, John F, Sohn, Yong Ho, Fea, Antonio, Ozaki, Mineo, Lai, Jimmy SM, Tantisevi, Visanee, Khaing, Chaw Chaw, Mizoguchi, Takanori, Nakano, Satoko, Kim, Chan-Yun, Tang, Guangxian, Fan, Sujie, Wu, Renyi, Meng, Hailin, Nguyen, Thi Thuy Giang, Tran, Tien Dat, Ueno, Morio, Martinez, Jose Maria, Ramli, Norlina, Aung, Yin Mon, Reyes, Rigo Daniel, Vernon, Stephen A, Fang, Seng Kheong, Xie, Zhicheng, Chen, Xiao Yin, Foo, Jia Nee, Sim, Kar Seng, Wong, Tina T, Quek, Desmond T, Venkatesh, Rengaraj, Kavitha, Srinivasan, Krishnadas, Subbiah R, Soumittra, Nagaswamy, Shantha, Balekudaru, Lim, Boon-Ang, Ogle, Jeanne, de Vasconcellos, José PC, Costa, Vital P, Abe, Ricardo Y, de Souza, Bruno B, and Sng, Chelvin C

Subjects
Male, Aging, Genotype, Human Genome, Chromosome Mapping, Gene Expression, Glaucoma, Neurodegenerative, Biological Sciences, Medical and Health Sciences, Cell Line, Angle-Closure, Genetic Loci, Genetics, Humans, Genetic Predisposition to Disease, Female, Eye Disease and Disorders of Vision, Genome-Wide Association Study, Developmental Biology
Abstract

Primary angle closure glaucoma (PACG) is a major cause of blindness worldwide. We conducted a genome-wide association study (GWAS) followed by replication in a combined total of 10,503 PACG cases and 29,567 controls drawn from 24 countries across Asia, Australia, Europe, North America, and South America. We observed significant evidence of disease association at five new genetic loci upon meta-analysis of all patient collections. These loci are at EPDR1 rs3816415 (odds ratio (OR) = 1.24, P = 5.94 × 10(-15)), CHAT rs1258267 (OR = 1.22, P = 2.85 × 10(-16)), GLIS3 rs736893 (OR = 1.18, P = 1.43 × 10(-14)), FERMT2 rs7494379 (OR = 1.14, P = 3.43 × 10(-11)), and DPM2-FAM102A rs3739821 (OR = 1.15, P = 8.32 × 10(-12)). We also confirmed significant association at three previously described loci (P < 5 × 10(-8) for each sentinel SNP at PLEKHA7, COL11A1, and PCMTD1-ST18), providing new insights into the biology of PACG.

Published
2016

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