Barnard W, Bower J, Brown M A, Murphy M, Austin L
Department of Biochemistry, Monash University, Clayton Victoria, Australia.
J Neurol Sci. 1994 May;123(1-2):108-13. doi: 10.1016/0022-510x(94)90211-9.
Leukemia inhibitory factor (LIF) is known to stimulate myoblast growth in culture via direct receptor mediated mechanisms, but it does not suppress myoblast fusion in vitro. We show here that LIF is also effective in vivo, using a muscle crush model. Administration of LIF to the site of the crush results in an increased rate of regeneration of the injured muscle. LIF stimulates an increase in the size of the muscle fibers rather than an increase in total number. Perfusion of 125I-labelled LIF (125I-LIF) at the site of the crush leads to uptake of the great majority of 125I-LIF into the muscle, which suggests that LIF is acting directly at the site of injury. Further, following crush injury LIF mRNA synthesis commences in the muscle. These data provide evidence that LIF is acting as a natural trauma factor in vivo and is actively involved in muscle regeneration.
已知白血病抑制因子（LIF）通过直接的受体介导机制刺激培养中的成肌细胞生长，但它在体外并不抑制成肌细胞融合。我们在此表明，利用肌肉挤压模型，LIF在体内也具有作用。将LIF施用于挤压部位会导致受损肌肉的再生速率增加。LIF刺激肌纤维大小增加，而非总数增加。在挤压部位灌注125I标记的LIF（125I-LIF）会使绝大多数125I-LIF被肌肉摄取，这表明LIF直接在损伤部位起作用。此外，挤压损伤后，肌肉中开始合成LIF mRNA。这些数据提供了证据，表明LIF在体内作为一种天然创伤因子，积极参与肌肉再生。
