Human Skeletal Muscle Progenitor Cells (Myoblasts)
Cat.No.: CSC-C3196
Species: Human
Source: Skeletal Muscle
Cell Type: Myoblast
- Specification
- Background
- Scientific Data
- Q & A
- Customer Review
Human Skeletal Muscle Progenitor Cells (myoblasts) are primarily derived from human skeletal muscle tissue. These cells, located within the skeletal muscle tissue, are key to muscle development and regeneration. Myoblasts usually exist in the basal layer of skeletal muscles and become activated by damage or stimuli which leads them to transform into mature muscle fibers. Myoblasts exist primarily in embryonic muscle tissues during fetal development but migrate to skeletal muscle regions after birth. Additionally, specific differentiation protocols enable human induced pluripotent stem cells (hiPSCs) to become myoblasts which serve as an in vitro research model.
Myoblasts primarily function to generate and regenerate skeletal muscle tissue. Myoblasts repair muscle damage by transforming into mature muscle fibers and creating skeletal muscle fibers throughout developmental processes. Furthermore, Myoblasts maintain muscle microenvironment homeostasis through the secretion of growth factors and extracellular matrix components. Myoblasts serve as valuable tools for in vitro and in vivo research into skeletal muscle degenerative diseases like muscular dystrophy and their treatment methods. In tissue engineering myoblasts can be integrated with biomaterials including Matrigel to develop three-dimensional models of muscle tissue that simulate muscle regeneration.
sPIF promotes myoblast differentiation and utrophin expression while inhibiting fibrosis in Duchenne muscular dystrophy via the H19/miR-675/let-7 and miR-21 pathways
Background
This study investigates synthetic preimplantation factor (sPIF) as a therapy for Duchenne muscular dystrophy. In mouse C2C12 cells and human myoblasts from healthy donors and DMD patients, sPIF promoted myogenic differentiation, reduced collagen 1A1/1A2 and TGF-β, and lowered fibrosis regulator miR-21. Mechanistically, sPIF upregulated lncRNA H19 and miR-675, downregulated let-7, and increased utrophin. In mdx mice, sPIF decreased serum creatine kinase and diaphragm collagen I/IV while increasing utrophin in diaphragm, heart, and quadriceps. These results support sPIF as a promising DMD therapeutic candidate.
Key Findings
sPIF promoted differentiation of mouse C2C12 and human myoblasts from healthy donors and DMD patients, increasing MyoD, myogenin, MyHC, troponin, and myotube fusion. In DMD myoblasts, sPIF inhibited fibrogenic differentiation, reducing collagen 1A1, collagen 1A2, and TGF-β, and decreased miR-21, a major fibrosis regulator. Mechanistically, sPIF upregulated lncRNA H19 and miR-675-3p/5p; H19 silencing or miR-675 antagomiRs abrogated sPIF-induced differentiation, while miR-675 mimics enhanced MyHC/troponin. sPIF increased utrophin via the H19/miR-675/let-7 axis: H19 sponges let-7, sPIF downregulated let-7, and let-7 overexpression blocked utrophin induction. In mdx mice, sPIF reduced serum creatine kinase and diaphragm collagen I/IV, and increased utrophin in diaphragm, heart, and quadriceps. These findings identify H19/miR-675/let-7 and miR-21 as mediators of sPIF benefits, supporting sPIF as a potential DMD therapy.
Contribution
Creative Bioarray supplied human myoblasts, including DMD patient-derived and healthy donor cells, as critical in vitro models. These cells enabled assessment of sPIF effects on myogenic differentiation, fibrogenic gene expression, miR-21, H19/miR-675, let-7, and utrophin, supporting the study's mechanistic and translational conclusions.
AAV Gene Transfer with Tandem Promoter Design Prevents Anti-transgene Immunity and Provides Persistent Efficacy in Neonate Pompe Mice
Background
This study describes tandem promoter monocistronic expression cassettes packaged in a single AAV vector that combine hepatic and extra-hepatic tissue-specific transgene expression to prevent anti-transgene immunity. Validated in infantile Pompe disease, the tandem liver-muscle promoter (LiMP) and liver-neuron promoter (LiNeuP) drove specific transgene expression in target tissues of immunocompetent Gaa−/− mice without eliciting anti-GAA antibodies. Neonatal AAV8 or AAV9 gene therapy with LiMP provided persistent therapeutic GAA expression and corrected glycogen accumulation, cardiomegaly and muscle strength at low vector doses.
Key Findings
Tandem promoters combining the liver ApoE-hAAT enhancer-promoter with the muscle spC5.12 promoter (LiMP) or the neuronal hSYN promoter (LiNeuP) were engineered within the <5 kb AAV packaging limit and verified in hepatocyte, myoblast and neuronal cell lines. Systemically delivered AAV vectors using LiMP or LiNeuP drove specific hGAA mRNA expression in liver plus muscle or CNS, respectively, and, unlike the ubiquitous CAG or muscle-only C5.12 promoters, prevented anti-hGAA IgG formation in adult immunocompetent Gaa−/− mice; LiMP also reduced pre-existing anti-GAA antibodies. In neonate Gaa−/− mice, AAV8- or AAV9-LiMP-sec-hGAA at doses 10–50-fold lower than previously reported produced persistent hepatic and muscle enzyme expression, supra-physiological muscle GAA activity, glycogen clearance in heart, diaphragm, triceps, quadriceps, spinal cord and brain, corrected cardiomegaly and rescued muscle strength without anti-GAA immunity, whereas single tissue-specific promoters or LiNeuP failed.
Contribution
Creative Bioarray provided the human skeletal muscle myoblasts (CSC-C3196) and the SuperCult Skeletal Muscle Cell Growth Medium Kit used to confirm in vitro that the tandem LiMP promoter retains transcriptional activity in human muscle cells, supporting translation of the tandem promoter design to human muscle.
ZIKV Replicates in Human Skeletal Muscle Progenitor Cells, Causing Cell Death
Zika virus (ZIKV) infections have raised global concerns due to severe neurological outcomes. While its neurotropic nature is well-known, the role of peripheral tissues in viral amplification is less explored. Gavino-Leooldino et al. aim to uncover the potential of skeletal muscle as an early ZIKV replication site, hypothesizing that muscle replication contributes to increased peripheral viral loads and later neural tissue invasion.
To assess whether muscle could be a ZIKV replication site, primary human skeletal muscle myoblasts (HSMM) were infected at the myoblast stage and as differentiated myotubes. Quantification of infectious particles (Fig. 1A) showed a rapid increase in ZIKV particles in myoblast cultures for at least 48 hours post-infection (hpi). Myotubes showed no increase until 16 hpi, but by 36 hpi, viral titers matched those in myoblasts. Immunostaining confirmed the presence of ZIKV E and NS2B proteins in myoblasts and myotubes at 36 hpi (Fig. 1B-E). No viral protein staining was seen in mock cultures. More ZIKV-positive cells were found in myoblast than myotube cultures at 36 and 48 hpi (Fig. 1H). Then, they assessed ZIKV replication's impact on skeletal muscle cell viability. At 48 hours post-infection (hpi), myoblast viability reduced by about 50%, whereas myotube viability remained unchanged (Fig. 1I). Consistently, myosin heavy chain (MF20) labeling showed no structural changes in myofibers of ZIKV-infected compared to mock-treated myotubes (Fig. 1F and 1G). Quantification confirmed unchanged fiber count and area (Fig. 1J), indicating ZIKV does not disrupt existing myofiber integrity. These findings suggest ZIKV replicates in myogenic cells, causing significant damage.
Fig. 3. ZIKV replicates and promotes death of human skeletal muscle progenitor cells.
USCIGF1 was Fused with Human and Mouse Skeletal Muscle Progenitor Cells in vitro.
Skeletal muscles, crucial for body function, often suffer injuries affecting health and mobility. Traditional muscle regeneration relies on satellite cells, but their scarcity after severe injuries limits recovery. Stem cell therapy emerges as a promising alternative. Urine-derived stem cells (USC), easily obtained non-invasively, have shown myogenic potential.
Yi's team used USCIGF1, created by lentivirus to overexpress IGF1, assessing its effects on muscle regeneration in a rodent model. Myofusion assays were conducted between mCherry-labeled USCIGF1 and hSMPCGFP (human skeletal muscle progenitor cells labeled with a GFP-containing plasmid). The number of fused cells increased significantly, reaching 23 fused myotubes per 2×105 USCIGF1 at a 1:2 ratio after 7 days of differentiation (Fig. 2A and B). Fusion was first seen 3 days after switching to differentiation media and persisted until Day 14. Human USCIGF1 fused distinctly with mSMPCGFP, confirmed by immunostaining for human mitochondria, lamin, and dystrophin 3 (DYS3) in myotubes (Fig. 2C). In contrast, only one myotube was detectable from USC and USCmCherry controls per 2×105 cells. Cytoplasm and mitochondria were observed in myotubes with mCherry-labeled USCIGF and hSMPCGFP (Fig. 2D). These results indicated IGF1 overexpression increased the ability of USC to fuse with skeletal myocytes to form myotubes.
Fig. 4. USCIGF1 was fused with human skeletal muscle progenitor cells (hSMPC) and mouse skeletal muscle progenitor cells (mSMPC) in vitro (Yi H, Chen G, et al., 2024).
Ask a Question
Write your own review
Description: Description: Human skeletal muscle cells are derived from whole muscle that has been dissociated into single cells and frozen. These muscle cells are from a single donor. They enable researchers to ...
Description: HSkMSC from Creative Bioarray are isolated from human muscle of the pectoral girdle. HSkMSC are cryopreserved at primary culture or passage one and delivered frozen. Each vial contains >5 x 10^5 ...
Description: Origin: HumanDesease: Duchenne Muscular Dystrophy (DMD)Application: These cells can be used for various types of in vitro, in vivo, or regenerative medicine studies in normal or diseased systems and ...
Description: Human Skeletal Muscle Microvascular Endothelial Cells are isolated from human skeletal muscle tissue.
Description: Diabetic Type I and Type II Human Skeletal Muscle Myoblasts (HSMM) are isolated from donors diagnosed with either Diabetes Type I or Diabetes Type II. Additional donor information is available by ...
Description: Diabetic Type I and Type II Human Skeletal Muscle Myoblasts (HSMM) are isolated from donors diagnosed with either Diabetes Type I or Diabetes Type II. Additional donor information is available by ...