脂肪组织是如何在受损伤的肌肉中堆积的？在1月在线出版的《自然—细胞生物学》期刊上，研究人员报告了他们对这一问题的看法。这种脂肪的沉积与肌肉营养失调等疾病有关，新研究有助于发展这类疾病的新治疗方法。
健康的肌肉再生依赖于多重细胞类型的反应，包括被称为成体肌肉干细胞的卫星细胞。Akiyoshi Uezumi和同事从卫星干细胞中鉴别出一组始祖细胞，这些卫星细胞在细胞培养液和小鼠中都能形成脂肪组织。这些PDGFRalpha+细胞在健康肌肉细胞中被抑制，但当被移植到小鼠受损伤的肌肉中后，却能够增生扩散。
在另一篇相关的论文中，Fabio Rossi和同事合作，鉴别出在肌肉组织中定居的脂肪所形成的始祖细胞。利用移植技术，他们发现这些细胞在被移植到受损害的组织中后会长出新的脂肪组织，却不会在小鼠的健康组织中生长。这些细胞不直接参与组织修复，但能刺激肌肉功能的恢复。
研究人员相信，以这些脂肪始祖细胞为靶标也许会打开一扇新的治疗方法大门，治疗肌肉疾病并减少疤痕。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature Cell Biology 17 January 2010 | doi:10.1038/ncb2014
Mesenchymal progenitors distinct from satellite cells contribute to ectopic fat cell formation in skeletal muscle
Akiyoshi Uezumi1, So-ichiro Fukada2, Naoki Yamamoto3, Shin'ichi Takeda4 & Kunihiro Tsuchida1
Ectopic fat deposition in skeletal muscle is closely associated with several disorders, however, the origin of these adipocytes is not clear, nor is the mechanism of their formation. Satellite cells function as adult muscle stem cells but are proposed to possess multipotency. Here, we prospectively identify PDGFRα+ mesenchymal progenitors as being distinct from satellite cells and located in the muscle interstitium. We show that, of the muscle-derived cell populations, only PDGFRα+ cells show efficient adipogenic differentiation both in vitro and in vivo. Reciprocal transplantations between regenerating and degenerating muscles, and co-culture experiments revealed that adipogenesis of PDGFRα+ cells is strongly inhibited by the presence of satellite cell-derived myofibres. These results suggest that PDGFRα+ mesenchymal progenitors are the major contributor to ectopic fat cell formation in skeletal muscle, and emphasize that interaction between muscle cells and PDGFRα+ mesenchymal progenitors, not the fate decision of satellite cells, has a considerable impact on muscle homeostasis.
1 Division for Therapies against Intractable Diseases, Institute for Comprehensive Medical Science, Fujita Health University, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi 470-1192, Japan.
2 Department of Immunology, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamada-oka, Suita, Osaka 565-0871, Japan.
3 Laboratory of Molecular Biology & Histochemistry, Fujita Health University Joint Research Laboratory, Aichi 470-1192, Japan.
4 Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8502, Japan.
