Muscle Cell News 1.29 October 24, 2016 | |
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TOP STORYInstrumented Cardiac Microphysiological Devices via Multimaterial Three-Dimensional Printing Researchers introduced a facile route for fabricating a new class of instrumented cardiac microphysiological devices via multimaterial three-dimensional printing. They further applied these devices to study drug responses, as well as the contractile development of human stem cell-derived laminar cardiac tissues over four weeks. [Nat Meter] Abstract | Press Release | Video | |
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PUBLICATIONS(Ranked by impact factor of the journal)CARDIAC MUSCLE CELLSNogo-C Regulates Cardiomyocyte Apoptosis during Mouse Myocardial Infarction Investigators found that Nogo-C was upregulated in mouse hearts after myocardial infarction, and hypoxic treatments also increased Nogo-C protein level in cardiomyocytes. [Cell Death Dis] Full Article The epicardium contributes signals and cells to the developing and adult injured heart and exploring strategies for modulating its activity is of great interest. Using inducible genetic mosaics, the authors overexpressed Myc in the epicardium and determined the differential expansion of Myc-overexpressing cells with respect to their wild type counterparts. [Sci Rep] Full Article The authors determined the effects of specifically and substantially depleting tat-interactive protein 60 (Tip60) from cardiomyocytes (CMs) using Kat5LoxP/-;Myh6-Cre mice in the absence of stress. The authors showed that chronic depletion of Tip60 from the ventricular myocardium beginning at early stages of neonatal heart development causes CM death after 8 weeks; hence, Tip60 protein has a crucial function in the heart. [PLoS One] Full Article Scientists examined the hypothesis that cardiosphere-derived cells favor heart repair by switching the macrophages from a pro-inflammatory phenotype (M1) into a regulatory anti-inflammatory phenotype (M2). [PLoS One] Full Article SKELETAL MUSCLE CELLSInvestigators showed that genetic disruption of the clock activator BMAL1 in skeletal myotubes and fibroblasts increased levels of the hypoxia-inducible factor 1α (HIF1α) under hypoxic conditions. [Cell Metab] Abstract | Press Release | Graphical Abstract NAD+ Repletion Improves Muscle Function in Muscular Dystrophy and Counters Global PARylation In diverse populations of normal healthy mice, the authors observed correlations between the abundance of mRNA transcripts related to mitochondrial biogenesis, the dystrophin-sarcoglycan complex, and nicotinamide adenine dinucleotide (NAD+) synthesis, consistent with a potential role for the essential cofactor NAD+ in protecting muscle from metabolic and structural degeneration. [Sci Transl Med] Abstract | Press Release Investigators demonstrated that the calcium- and voltage-dependent potassium channel, KCa1.1 (BK, Slo1, KCNMA1), regulates myoblast proliferation, migration, and fusion. They also showed a loss of plasma membrane expression of the pore-forming α subunit of KCa1.1 in myotonic dystrophy type 1 myoblasts. [Cell Death Dis] Full Article Dnmt1 Regulates the Myogenic Lineage Specification of Muscle Stem Cells Scientists showed that Dnmt1 is required for myogenesis. Loss of Dnmt1 results in reduced expression of myogenic genes and defects in myogenic differentiation. They utilized a conditional knockout mouse approach to examine the functional consequences of Dnmt1 depletion specifically in the developing muscle. [Sci Rep] Full Article The histone 3 lysine 9 methyltransferase Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on the roles of Setdb1 in these mutually exclusive processes, the authors used mouse skeletal myoblasts as a model of terminal differentiation. [Cell Discov] Full Article SMOOTH MUSCLE CELLSIn vascular smooth muscle cells (VSMCs), stimulation of TRPC1-based SOCs mediate Ca2+ entry pathways which regulate contractility, proliferation and migration. The authors investigated how store depletion stimulates this gating pathway. Store-operated TRPC1 channel activity was inhibited by TRPC1 and STIM1 antibodies and STIM1 shRNA in wild-type VSMCs, and was absent in TRPC1−/− VSMCs. [J Physiol] Abstract The authors identified endophilin A2 as a ClC-3 channel partner, which serves as a new ClC-3 trafficking insight in regulating volume-regulated Cl– current in vascular smooth muscle cells (VSMCs). This study provides a new mechanism by which endophilin A2 regulates ClC-3 channel activity, and sheds light on how ClC-3 is transported to cell membranes to play its critical role as a chloride channel in VSMCs function, which may be involved in cardiovascular diseases. [Circ J] Full Article | |
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REVIEWSExercise-Stimulated Glucose Uptake — Regulation and Implications for Glycemic Control The authors review the molecular mechanisms that regulate the movement of glucose from the capillary bed into the muscle cell and discuss what is known about their integrated regulation during exercise. [Nat Rev Endocrinol] Abstract Visit our reviews page to see a complete list of reviews in the muscle cell research field. | |
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INDUSTRY NEWSaTyr Pharma, Inc. announced that its product candidate Resolaris™ was granted Fast Track designation by the US Food and Drug Administration (FDA) for the treatment of FSHD, making it the first known therapeutic candidate for the treatment of FSHD to receive the designation. [aTyr Pharma, Inc.] Press Release Solid Biosciences and its subsidiary, Solid GT, announced that the U.S. Food and Drug Administration and the European Commission have granted Orphan Drug designations for the company’s gene therapy candidate, SGT-001, for the treatment of patients with Duchenne muscular dystrophy. [Solid Biosciences LLC] Press Release | |
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POLICY NEWSReview Finds Misconduct in Events Surrounding WHO Fetal Growth Study For the first time in its 68-year history, the World Health Organization (WHO) has concluded that researchers are guilty of research misconduct. An independent review commissioned by WHO has found that “research ethics misconduct occurred” in a multimillion-dollar global study on fetal growth led by researchers at the University of Oxford in the United Kingdom. [ScienceInsider] Editorial Two Major California Research Institutes Will Merge One of the biggest nonprofit biomedical research outfits in the world is getting a new translational medicine research arm, aimed at speeding the conversion of basic research insights into novel medicines. Officials at the Scripps Research Institute announced that it will merge with the California Institute for Biomedical Research, which was launched in 2012 as a nonprofit version of a drug development company. [ScienceInsider] Editorial To Save Money, NSF Requires University Cost-Sharing for Rotators The National Science Foundation (NSF) has decided that universities should pay 10% of the salaries of faculty members working temporarily at the agency. NSF hopes the new policy will demonstrate its commitment to saving taxpayer dollars without alienating the academic community that it relies upon to stay on the cutting edge of basic science. [ScienceInsider] Editorial
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EVENTSNEW Challenges, Solutions and Progress in Stem Cell Medicine Visit our events page to see a complete list of events in the community.
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JOB OPPORTUNITIESNEW Research Associate – Craniofacial Development and Stem Cell Biology (King’s College London) NEW Assistant Professor – Biomedical Engineering (Univesrity of South Dakota) Faculty Position (Tenure) – Cardiovascular Biology (University of Maryland School of Medicine) National Field Product Service Specialist (Cook MyoSite) Research and Development Specialist- Muscle Stem Cell (Nestlé Institute of Health Sciences) Postdoctoral Position – Lipid Metabolism (Baylor College of Medicine) Chair – Medical Biology (Masaryk University) Recruit Top Talent: Reach potential candidates by posting your organization’s career opportunities on the Connexon Creative Job Board at no cost.
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Home Muscle Cell News Volume 1.29 | Oct 24 2016