Regular ArticleIn Vivo Migration of Transplanted Myoblasts Requires Matrix Metalloproteinase Activity
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Human myoblasts differentiate in various mesenchymal lineages and inhibit allogeneic T cell proliferation through an indolamine 2,3 dioxygenase dependent pathway
2021, Experimental Cell ResearchCitation Excerpt :However, subsequent clinical trials in humans, did not confirm the preclinical observations [5,6]. These disappointing results were explained in part by the poor survival and limited migratory aptitude of injected cells in patients [7–9]. Other cellular sources were considered for muscle cell therapy including mesoangioblasts [10–12], pluripotent stem cells [13,14] and CD133+ myogenic stem cells [15–17], all demonstrating high regenerative potential in animal models.
Cellular Biomechanics in Skeletal Muscle Regeneration
2018, Current Topics in Developmental BiologyMechanosensing of matrix by stem cells: From matrix heterogeneity, contractility, and the nucleus in pore-migration to cardiogenesis and muscle stem cells in vivo
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2017, Comprehensive Biomaterials IIThe role of matrix metalloproteinases in muscle and adipose tissue development and meat quality: A review
2016, Meat ScienceCitation Excerpt :Alameddine (2012) observed MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, MMP-10, MMP-14 and MMP-16 in myogenic cells of various species. Other studies have also indicated an important role of MMP-2, MMP-7, MMP-9 and MT1-MMP in myotube formation (El Fahime, Torrente, Caron, Bresolin, & Tremblay, 2000; Lewis, Tippett, Sinanan, Morgan, & Hunt, 2000 and Caron, Asselin, Morel, & Tremblay, 1999) and Lluri and Jaworski (2005) confirmed that TIMP-2, MT1-MMP, and MMP-2 are upregulated coincident with myogenesis. MMPs are responsible for the degradation of intramuscular connective tissue to allow an appropriate increase in muscle fiber size when the muscle increases the size during growth of the animal (Purslow, 2005).
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