Helgren Maureen E, Squinto Stephen P, Davis Heather L, Parry David J, Boulton Teri G, Heck Carol S, Zhu Yuan, Yancopoulos George D, Lindsay Ronald M, DiStefano Peter S
Regeneron Pharmaceuticals, Incorporated, Tarrytown, New York 10591.
Cell. 1994 Feb 11;76(3):493-504. doi: 10.1016/0092-8674(94)90113-9.
The actions and receptor for ciliary neurotrophic factor (CNTF) are largely restricted to cells of the nervous system, although one of the CNTF receptor components, CNTFR alpha, is expressed by skeletal muscle. Here we show that the other CNTF receptor components, LIFR beta and gp130, are also expressed by skeletal muscle and that expression of all three CNTF receptor components is greatly increased in denervated muscle. In vivo, administration of CNTF activates these receptors on skeletal muscle by inducing receptor phosphorylation and immediate-early gene responses. Furthermore, CNTF reduces the denervation-induced atrophy of muscle and attenuates the reduced twitch and tetanic tensions that result from muscle denervation. Our findings reveal that, in addition to its known neurotrophic actions, CNTF exerts myotrophic effects by attenuating the morphological and functional changes associated with denervation of rat skeletal muscle.
睫状神经营养因子（CNTF）的作用和受体主要局限于神经系统的细胞，尽管CNTF受体成分之一，即CNTFRα，由骨骼肌表达。我们在此表明，其他CNTF受体成分，即白血病抑制因子受体β（LIFRβ）和糖蛋白130（gp130），也由骨骼肌表达，并且在去神经支配的肌肉中，所有这三种CNTF受体成分的表达都大幅增加。在体内，给予CNTF可通过诱导受体磷酸化和即刻早期基因反应来激活骨骼肌上的这些受体。此外，CNTF可减少去神经支配诱导的肌肉萎缩，并减轻因肌肉去神经支配导致的肌肉抽搐和强直张力降低。我们的研究结果表明，除了其已知的神经营养作用外，CNTF还通过减轻与大鼠骨骼肌去神经支配相关的形态和功能变化发挥肌营养作用。
