The San Diego Skeletal Muscle Research Center (SDMRC) is composed of 21 scientists who span five research institutions and nine academic Departments. The mission of the SDMRC is twofold: (1) to provide investigators with an effective infrastructure and environment to accelerate their cutting-edge research in an efficient and cost-effective manner, and (2) to provide an organizational structure that enhances communication amongst members and provides education and training for the San Diego community. The creation of this Center will integrate, educate and synergize laboratories on a more formalized basis than currently exists. Specifically, this Center will provide a mechanism for rapidly performing common assays needed by all investigators with minimal overhead in terms of time and money by creating three Cores: Phenotyping, Imaging, and High Throughput Cell Analysis. This will automatically enhance each of the individual programs since state-of-the-art methods will instantly become available to members. Access to new methods will undoubtedly spawn new ideas that accompany the experimental data. SDMRC will increase efficiency (since a mechanism is in place to collaborate and share information) and productivity (since studies will be routinely multidisciplinary) that will enable individuals to have a larger impact in their individual research programs than would be possible in isolation.

Public Health Relevance

Skeletal muscle research is necessarily translational since muscle diseases compromise quality of life, mobility, and overall health. Numerous diseases can be primarily or secondarily attributable to muscle problems which include primary myopathies such as the muscular dystrophies and also the secondary effects of muscle disease that lead to fragility, osteoporosis, obesity, diabetes and aging. The routine direct access to human muscle tissue in the operating room and in the clinic instantly provides extremely valuable tissue to all Center investigators using animal models of disease and this will insure that the work in this Core maintains clinical relevance since the results from model systems can be 'calibrated' against the actual disease itself.

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Center Core Grants (P30)
Project #
5P30AR061303-05
Application #
8915477
Study Section
Special Emphasis Panel (ZAR1-KM (M1))
Program Officer
Boyce, Amanda T
Project Start
2011-09-01
Project End
2016-08-31
Budget Start
2015-09-01
Budget End
2016-08-31
Support Year
5
Fiscal Year
2015
Total Cost
$673,342
Indirect Cost
$117,553
Name
University of California San Diego
Department
Orthopedics
Type
Schools of Medicine
DUNS #
804355790
City
La Jolla
State
CA
Country
United States
Zip Code
92093
Madaro, Luca; Passafaro, Magda; Sala, David et al. (2018) Denervation-activated STAT3-IL-6 signalling in fibro-adipogenic progenitors promotes myofibres atrophy and fibrosis. Nat Cell Biol 20:917-927
Diez-Cuñado, Marta; Wei, Ke; Bushway, Paul J et al. (2018) miRNAs that Induce Human Cardiomyocyte Proliferation Converge on the Hippo Pathway. Cell Rep 23:2168-2174
Liu, Eva S; Martins, Janaina S; Zhang, Wanlin et al. (2018) Molecular analysis of enthesopathy in a mouse model of hypophosphatemic rickets. Development 145:
Sartorelli, Vittorio; Puri, Pier Lorenzo (2018) Shaping Gene Expression by Landscaping Chromatin Architecture: Lessons from a Master. Mol Cell 71:375-388
Marroncelli, Nicoletta; Bianchi, Marzia; Bertin, Marco et al. (2018) HDAC4 regulates satellite cell proliferation and differentiation by targeting P21 and Sharp1 genes. Sci Rep 8:3448
Gibbons, Michael C; Singh, Anshuman; Engler, Adam J et al. (2018) The role of mechanobiology in progression of rotator cuff muscle atrophy and degeneration. J Orthop Res 36:546-556
Gokhin, David S; Fowler, Velia M (2017) Software-based measurement of thin filament lengths: an open-source GUI for Distributed Deconvolution analysis of fluorescence images. J Microsc 265:11-20
Jordan, Sabine D; Kriebs, Anna; Vaughan, Megan et al. (2017) CRY1/2 Selectively Repress PPAR? and Limit Exercise Capacity. Cell Metab 26:243-255.e6
Roberts, Thomas C; Etxaniz, Usue; Dall'Agnese, Alessandra et al. (2017) BRD3 and BRD4 BET Bromodomain Proteins Differentially Regulate Skeletal Myogenesis. Sci Rep 7:6153
Latella, Lucia; Dall'Agnese, Alessandra; Boscolo, Francesca Sesillo et al. (2017) DNA damage signaling mediates the functional antagonism between replicative senescence and terminal muscle differentiation. Genes Dev 31:648-659

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