Muscle Cell News 3.29 August 27, 2018 | |
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TOP STORYResearchers showed that NF-κB was activated in murine dystrophic hearts, and that cardiomyocyte ablation of NF-κB rescued cardiac function. This physiological improvement was associated with a signature of upregulated calcium genes, coinciding with global enrichment of permissive H3K27 acetylation chromatin marks and depletion of the transcriptional repressors CCCTC-binding factor, SIN3 transcription regulator family member A, and histone deacetylase 1. [Nat Commun] Full Article | |
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PUBLICATIONS(Ranked by impact factor of the journal)CARDIAC MUSCLE CELLSChannelopathy as a SUDEP Biomarker in Dravet Syndrome Patient-Derived Cardiac Myocytes Generation of a CRISPR gene-edited heterozygous SCN1A deletion in control induced pluripotent stem cells (iPSCs) increased sodium current density in iPSC-cardiac myocytes similar to that seen in patient cells. [Stem Cell Reports] Full Article | Press Release Investigators showed that damage-regulated autophagy modulator 1 (DRAM1) overexpression restored autophagic flux by enhancing autophagosome conversion to autophagolysosome. Although Atg12 mRNA was up-regulated with DRAM1 overexpression the free Atg12 protein was decreased accompanied by increased Atg12-Atg5 conjugate both in vitro and in vivo. [J Mol Cell Cardiol] Abstract Co-treatment of H9c2(2-1) cells with phenylephrine (PE) and fenofibrate restricted increase in cell size and expression of marker genes such as atrial-natriuretic peptide, brain-natriuretic peptide and β-myosin heavy chain compared to those with PE alone. [Cell Physiol Biochem] Full Article SKELETAL MUSCLE CELLSExon Skipping in a Dysf-Missense Mutant Mouse Model Researchers generated a new mouse model carrying a missense mutation in exon 38 in analogy to a clinically relevant human dysferlin (DYSF) variant. The targeted mutation induced all characteristics of missense mutant dysferlinopathy including a progressive dystrophic pattern, amyloid formation and defects in membrane repair. [Mol Ther Nucleic Acids] Abstract | Full Article Mice lacking cyclin D3 displayed an increased number of myofibers with higher oxidative capacity in fast-twitch muscle groups, primarily composed of myofibers that utilize glycolytic metabolism. Cyclin D3 could repress the calcineurin- or MEF2-dependent activation of a slow fiber-specific promoter in cultured muscle cells. [Sci Rep] Full Article CBP or P300 knockdown strongly impaired muscle cell adhesion and resulted in the activation of inflammation markers, two hallmarks of dystrophic disease. This was further validated in zebrafish where inhibition of CBP and P300 enzymatic activities led to cell adhesion defects and muscle fiber detachment. [Sci Rep] Full Article Visualization of PAX7 Protein Dynamics in Muscle Satellite Cells in a YFP Knock-in-Mouse Line The authors reported a knock-in mouse line expressing a PAX7-enhanced yellow fluorescent protein (YFP) fusion protein that enabled visualization of PAX7 protein dynamics in living satellite cells through YFP fluorescence. [Skelet Muscle] Full Article SMOOTH MUSCLE CELLSSilencing NEAT1 in vascular smooth muscle cells (VSMCs) resulted in enhanced expression of SM-specific genes while attenuating VSMC proliferation and migration. Researchers demonstrated that NEAT1 sequestered the key chromatin modifier WD repeat domain 5 from SM-specific gene loci, thereby initiating an epigenetic “off” state, resulting in down-regulation of SM-specific gene expression. [Proc Natl Acad Sci USA] Abstract Calcineurin phosphatase activity and nuclear translocation of nuclear factor of activated T-cells (NFAT) c2-4 were increased in pulmonary artery smooth muscle cells (PASMCs) derived from monocrotaline-treated rats. PASMC proliferation and migration were markedly inhibited in a dosedependent manner by cyclosporin A. [Cell Physiol Biochem] Full Article Transforming growth factor-β1 (TGF-β1) upregulated miR-21 expression by activating Smad2/3, and this in turn downregulated forkhead box O1 mRNA expression. TGF-β1-Smad-miR-21 signaling also downregulated phosphatase and tensin homolog deleted on chromosome ten expression and thus de-repressed the PI3K-Akt pathway. [J Cell Physiol] Abstract Lysosomal Membrane Permeabilization Causes Secretion of IL-1β in Human Vascular Smooth Muscle Cells Lysosomal membrane permeabilization (LMP) had both priming and activating roles, causing an upregulation of proIL-1β and NLRP3 and the secretion of mature IL-1β from unprimed human vascular smooth muscle cells. LMP activated the canonical NF-κB pathway. The priming effect of LMP was inhibited by CA-074 Me, indicating an upstream role of cathepsin B. [Inflamm Res] Full Article Subscribe to one of our other 19 science newsletters such as Extracellular Matrix News & ESC & iPSC News. | |
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REVIEWSEndocrine Crosstalk between Skeletal Muscle and the Brain The authors discuss the current stage of knowledge regarding how exercise and the muscle secretome improve a broad range of brain functions related to vascularization, neuroplasticity, memory, sleep and mood. [Front Neurol] Full Article Visit our reviews page to see a complete list of reviews in the muscle cell research field. | |
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INDUSTRY NEWSAudentes Therapeutics, Inc. announced that the U.S. FDA granted RMAT designation to AT132 for the treatment of X-linked Myotubular Myopathy (XLMTM). RMAT designation for AT132 was granted based on positive interim clinical data from ASPIRO, the ongoing Phase I/II clinical study of AT132 for XLMTM. [Audentes Therapeutics Inc.] Press Release Berlin Cures announced the successful completion of its Phase I study of BC 007, a DNA-based aptamer compound that binds to and eliminates functional pathogenic autoantibodies for the treatment of cardiomyopathy. [Berlin Cures GmbH] Press Release Muscular Dystrophy Association Announces 34 New Research Grants Totaling $9.9 Million The Muscular Dystrophy Association (MDA) announced the award of 34 new grants totaling $9.9 million for its Summer 2018 grant cycle. These new grants represent a continued commitment by MDA to fund groundbreaking research that will one day lead to treatments and cures for the diseases in its program. [Muscular Dystrophy Association Inc.] Press Release | |
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POLICY NEWSMassive £30-Million Grant Will Be Awarded to One Cardiovascular Research Team A lucky group of researchers will soon walk away with £30 million (US$39 million) to study the heart and circulatory system — one of the largest single grants for medical research in the world. The British Heart Foundation launched the award on 25 August, and it is open to international applicants. [Nature News] Editorial No-Deal Brexit ‘Worse than Thought’ for Science The impact of a no-deal Brexit on British science could be worse than previously thought, according to a new analysis. The campaign group Scientists for EU has studied the Brexit technical notes released by the government. One of the documents states the UK would no longer be eligible for three of the EU’s major funding programs. [The BBC] Editorial To Highlight Gender Gaps, Scientists Decline Opportunities Activists are protesting imbalanced conferences, editorial boards, and other professional activities by refusing to join. When neuroscientist Rogier Kievit was invited to join a journal’s editorial board, he took a look at the skewed gender ratio of its current members—21 men and 3 women—and said no thanks. [The Scientist] Editorial
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EVENTSNEW 7th Annual International Symposium on Regenerative Rehabilitation Visit our events page to see a complete list of events in the community.
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JOB OPPORTUNITIESNEW Postdoctoral Position – Genome Editing in Muscular Dystrophies (GENETHON) Postdoctoral Position – Duchenne Muscular Dystrophy Research (Leiden University Medical Center) Scientist – Cardiovascular Research (University of Iowas Hospital and Clinics) Postdoctoral Position – Duchenne Muscular Dystrophy Research (GENETHON) Postdoctoral Associate – Muscle Cell Research (University of Louisville) Postdoctoral Fellow – Immunoengineering for Muscle Regeneration (Duke University) Postdoctoral Fellow – Human Skeletal Muscle Disease Modeling and Regeneration (Duke University) Postdoctoral Fellow – hiPSC Based Cardiac Regeneration (Duke University) Postdoctoral Fellow – Cardiovascular Tissue Engineering (Stanford 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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