Liaw, Norman Yu Hui

[["dc.bibliographiccitation.firstpage","6427"],["dc.bibliographiccitation.journal","International Journal of Nanomedicine"],["dc.bibliographiccitation.lastpage","6428"],["dc.bibliographiccitation.volume","Volume 16"],["dc.contributor.author","Kittana, Naim"],["dc.contributor.author","Assali, Mohyeddin"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Liaw, Norman"],["dc.contributor.author","Santos, Gabriela Leao"],["dc.contributor.author","Rehman, Abdul"],["dc.contributor.author","Lutz, Susanne"],["dc.date.accessioned","2022-06-08T07:57:29Z"],["dc.date.available","2022-06-08T07:57:29Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.2147/IJN.S339659"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/110104"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-575"],["dc.relation.eissn","1178-2013"],["dc.title","Modulating the Biomechanical Properties of Engineered Connective Tissues by Chitosan-Coated Multiwall Carbon Nanotubes [Corrigendum]"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","156"],["dc.bibliographiccitation.journal","Advanced Drug Delivery Reviews"],["dc.bibliographiccitation.lastpage","160"],["dc.bibliographiccitation.volume","96"],["dc.contributor.author","Liaw, Norman Yu"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2017-09-07T11:54:43Z"],["dc.date.available","2017-09-07T11:54:43Z"],["dc.date.issued","2016"],["dc.description.abstract","Recreating the beating heart in the laboratory continues to be a formidable bioengineering challenge. The fundamental feature of the heart is its pumping action, requiring considerable mechanical forces to compress a blood filled chamber with a defined in- and outlet Ventricular output crucially depends on venous loading of the ventricles (preload) and on the force generated by the preloaded ventricles to overcome arterial blood pressure (afterload). The rate of contraction is controlled by the spontaneously active sinus node and transmission of its electrical impulses into the ventricles. The underlying principles for these physiological processes are described by the Frank-Starling mechanism and Bowditch phenomenon. It is essential to consider these principles in the design and evaluation of tissue engineered myocardium. This review focuses on current strategies to evoke mechanical loading in hydrogel-based heart muscle engineering. (C) 2015 Published by Elsevier B.V."],["dc.identifier.doi","10.1016/j.addr.2015.09.001"],["dc.identifier.gro","3141744"],["dc.identifier.isi","000370095000012"],["dc.identifier.pmid","26362920"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/591"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/92"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.eissn","1872-8294"],["dc.relation.issn","0169-409X"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Mechanical stimulation in the engineering of heart muscle"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","overview_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","597"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","611"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","del Campo, Cristina Villa"],["dc.contributor.author","Liaw, Norman Y."],["dc.contributor.author","Gunadasa-Rohling, Mala"],["dc.contributor.author","Matthaei, Moritz"],["dc.contributor.author","Braga, Luca"],["dc.contributor.author","Kennedy, Tahnee"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Giacca, Mauro"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Riley, Paul Richard"],["dc.date.accessioned","2022-04-01T10:00:36Z"],["dc.date.available","2022-04-01T10:00:36Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Aims After a myocardial infarction, the adult human heart lacks sufficient regenerative capacity to restore lost tissue, leading to heart failure progression. Finding novel ways to reprogram adult cardiomyocytes into a regenerative state is a major therapeutic goal. The epicardium, the outermost layer of the heart, contributes cardiovascular cell types to the forming heart and is a source of trophic signals to promote heart muscle growth during embryonic development. The epicardium is also essential for heart regeneration in zebrafish and neonatal mice and can be reactivated after injury in adult hearts to improve outcome. A recently identified mechanism of cell–cell communication and signalling is that mediated by extracellular vesicles (EVs). Here, we aimed to investigate epicardial signalling via EV release in response to cardiac injury and as a means to optimize cardiac repair and regeneration. Methods and results We isolated epicardial EVs from mouse and human sources and targeted the cardiomyocyte population. Epicardial EVs enhanced proliferation in H9C2 cells and in primary neonatal murine cardiomyocytes in vitro and promoted cell cycle re-entry when injected into the injured area of infarcted neonatal hearts. These EVs also enhanced regeneration in cryoinjured engineered human myocardium (EHM) as a novel model of human myocardial injury. Deep RNA-sequencing of epicardial EV cargo revealed conserved microRNAs (miRs) between human and mouse epicardial-derived exosomes, and the effects on cell cycle re-entry were recapitulated by administration of cargo miR-30a, miR-100, miR-27a, and miR-30e to human stem cell-derived cardiomyocytes and cryoinjured EHM constructs. Conclusion Here, we describe the first characterization of epicardial EV secretion, which can signal to promote proliferation of cardiomyocytes in infarcted mouse hearts and in a human model of myocardial injury, resulting in enhanced contractile function. Analysis of exosome cargo in mouse and human identified conserved pro-regenerative miRs, which in combination recapitulated the therapeutic effects of promoting cardiomyocyte proliferation."],["dc.identifier.doi","10.1093/cvr/cvab054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105469"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.title","Regenerative potential of epicardium-derived extracellular vesicles mediated by conserved miRNA transfer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","eaap9004"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Science Advances"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Long, Chengzu"],["dc.contributor.author","Li, Hui"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Rodriguez-Caycedo, Cristina"],["dc.contributor.author","Kyrychenko, Viktoriia"],["dc.contributor.author","Zhou, Huanyu"],["dc.contributor.author","Zhang, Yu"],["dc.contributor.author","Min, Yi-Li"],["dc.contributor.author","Shelton, John M."],["dc.contributor.author","Mammen, Pradeep P. A."],["dc.contributor.author","Liaw, Norman Y."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Bassel-Duby, Rhonda"],["dc.contributor.author","Schneider, Jay W."],["dc.contributor.author","Olson, Eric N."],["dc.date.accessioned","2018-04-23T11:49:13Z"],["dc.date.available","2018-04-23T11:49:13Z"],["dc.date.issued","2018"],["dc.description.abstract","Genome editing with CRISPR/Cas9 is a promising new approach for correcting or mitigating disease-causing mutations. Duchenne muscular dystrophy (DMD) is associated with lethal degeneration of cardiac and skeletal muscle caused by more than 3000 different mutations in the X-linked dystrophin gene (DMD). Most of these mutations are clustered in “hotspots.” There is a fortuitous correspondence between the eukaryotic splice acceptor and splice donor sequences and the protospacer adjacent motif sequences that govern prokaryotic CRISPR/Cas9 target gene recognition and cleavage. Taking advantage of this correspondence, we screened for optimal guide RNAs capable of introducing insertion/deletion (indel) mutations by nonhomologous end joining that abolish conserved RNA splice sites in 12 exons that potentially allow skipping of the most common mutant or out-of-frame DMD exons within or nearby mutational hotspots. We refer to the correction of DMD mutations by exon skipping as myoediting. In proof-of-concept studies, we performed myoediting in representative induced pluripotent stem cells from multiple patients with large deletions, point mutations, or duplications within the DMD gene and efficiently restored dystrophin protein expression in derivative cardiomyocytes. In three-dimensional engineered heart muscle (EHM), myoediting of DMD mutations restored dystrophin expression and the corresponding mechanical force of contraction. Correcting only a subset of cardiomyocytes (30 to 50%) was sufficient to rescue the mutant EHM phenotype to near-normal control levels. We conclude that abolishing conserved RNA splicing acceptor/donor sites and directing the splicing machinery to skip mutant or out-of-frame exons through myoediting allow correction of the cardiac abnormalities associated with DMD by eliminating the underlying genetic basis of the disease."],["dc.identifier.doi","10.1126/sciadv.aap9004"],["dc.identifier.gro","3142510"],["dc.identifier.pmid","29404407"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13664"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/202"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A08: Translationale und posttranslationale Kontrolle trunkierter Titinproteine in Kardiomyozyten von Patienten mit dilatativer Kardiomyopathie"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.issn","2375-2548"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Correction of diverse muscular dystrophy mutations in human engineered heart muscle by single-site genome editing"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]