骨骼肌通过单核成肌前体细胞——肌母细胞的增殖来实现再生，这些肌母细胞最终融合并整合成多核的肌管，随后这些肌管成熟为肌纤维。该过程不仅发生于胚胎时期的肌肉组织发生，也发生在出生后因损伤引起的肌肉再生过程中，或见于如杜氏肌营养不良症等疾病中。肌母细胞的融合是骨骼肌特有的过程，未形成肌纤维的肌母细胞将分化为卫星细胞。骨骼肌肌母细胞表达 FGF 受体，且在培养过程中分化时 IGF 的表达水平会上升。人类骨骼肌肌母细胞培养是一种便捷的体外模型，可用于研究细胞发育与分化、胰岛素代谢以及组织修复。
ScienCell Research Laboratories 提供的 HSkMM 来源于人体胸带肌肉。HSkMM 在第一代时经冷冻保存，并以冷冻形式运输。每个冻存管含有超过 5 x 105 个细胞，体积为 1 毫升。HSkMM 通过针对肌球蛋白和/或肌动蛋白的抗体进行免疫荧光鉴定。HSkMM 经检测为 HIV-1、HBV、HCV、支原体、细菌、酵母菌和真菌阴性。在 ScienCell Research Laboratories 提供的条件下，HSkMM 可保证扩增至少 15 次群体倍增。
推荐培养基
建议使用 Skeletal Muscle Cell Medium（SkMCM，目录号 #3501）进行体外培养 HSkMM。
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Type 2 diabetes (T2D) is characterized by impaired glucose uptake in skeletal muscle and adipose tissues, which contributes to systemic hyperglycemia. GLUT4 is a crucial ... More
Type 2 diabetes (T2D) is characterized by impaired glucose uptake in skeletal muscle and adipose tissues, which contributes to systemic hyperglycemia. GLUT4 is a crucial component in insulin-stimulated glucose uptake, and its expression and translocation are impaired in T2D onset. This study explored the role of extracellular vesicles (EVs) derived from GLUT4-overexpressing engineered muscle constructs (G4OE-EMC) in glucose metabolism. G4OE-EMC-derived EVs enhanced glucose uptake and insulin sensitivity both in vitro, when tested on wild-type (WT) engineered muscle constructs, and in vivo, using the diet-induced obesity (DIO) mouse model. Proteomic and transcriptomic analyses revealed that the EVs were enriched in IGF1 and contained reduced levels of miRNAs, such as miR-122-5p, miR-16-5p, and miR-486-5p, which target IGF1R. The multiomic approach used here combined with in vivo and in vitro results suggest a mechanism whereby G4OE-derived EVs enhance glucose metabolism via IGF1 signaling and miRNA-mediated regulation of IGF1R expression, offering a path for potential therapeutic strategy for T2D. Less
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