Nomura Tetsuya, Ashihara Eishi, Tateishi Kento, Asada Satoshi, Ueyama Tomomi, Takahashi Tomosaburo, Matsubara Hiroaki, Oh Hidemasa
Department of Experimental Therapeutics, Translational Research Center, Kyoto University Hospital, Kyoto 606-8507, Japan.
Biochem Biophys Res Commun. 2007 Jan 19;352(3):668-74. doi: 10.1016/j.bbrc.2006.11.097. Epub 2006 Nov 27.
Bone marrow cells have been shown to contribute to neovascularization in ischemic hearts, whereas their impaired maturation to restore the delta-sarcoglycan (delta-SG) expression responsible for focal myocardial degeneration limits their utility to treat the pathogenesis of cardiomyopathy. Here, we report the isolation of multipotent progenitor cells from adult skeletal muscle, based on their ability to generate floating-myospheres. Myosphere-derived progenitor cells (MDPCs) are distinguishable from myogenic C2C12 cells and differentiate into vascular smooth muscle cells and mesenchymal progeny. The mutation in the delta-SG has been shown to develop vascular spasm to affect sarcolemma structure causing cardiomyopathy. We originally generated delta-SD knockdown (KD) mice and transplanted MDPCs into the hearts. MDPCs enhanced neoangiogenesis and restored delta-SG expression in impaired vasculatures through trans-differentiation, leading to improvement of cardiac function associated with paracrine effectors secretion. We propose that MDPCs may be the promising progenitor cells in skeletal muscle to treat delta-sarcoglycan complex mutant cardiomyopathy.
骨髓细胞已被证明有助于缺血性心脏的新血管形成,然而,它们成熟受损,无法恢复负责局灶性心肌变性的δ-肌聚糖(δ-SG)表达,这限制了它们在治疗心肌病发病机制方面的效用。在此,我们报告基于其生成漂浮肌球的能力,从成年骨骼肌中分离出多能祖细胞。肌球衍生的祖细胞(MDPCs)与成肌C2C12细胞不同,可分化为血管平滑肌细胞和间充质后代。已证明δ-SG中的突变会引发血管痉挛,影响肌膜结构,从而导致心肌病。我们最初构建了δ-SG基因敲低(KD)小鼠,并将MDPCs移植到心脏中。MDPCs通过转分化增强了新生血管形成,并恢复了受损血管系统中的δ-SG表达,导致与旁分泌效应物分泌相关的心脏功能改善。我们认为MDPCs可能是骨骼肌中治疗δ-肌聚糖复合物突变型心肌病的有前景的祖细胞。