TY - JOUR
T1 - Rescue of motoneurons from cell death by a purified skeletal muscle polypeptide
T2 - Effects of the ChAT development factor, CDF
AU - McManaman, James L.
AU - Oppenheim, Ronald W.
AU - Prevette, David
AU - Marchetti, Dario
N1 - Funding Information:
This work was supported by grants from the National Institutes of Health and the Muscular Dystrophy Association. D. M. was supported by NIH training grant No. USPH 5T32NS07182-10. We would like to thank Dr. F. Fuller for human recombinant bFCF and Drs. S. H. Appel, L. 1. Haverkamp, and J. Patrick for their comments on the manuscript and for many helpful discussions. We would also like to thank F. Crawford and R. Clark for their excellent technical assistance and the Department of Neurology Word Processing Center for help in the preparation of the manuscript. This is publication No. 4 from the Wagner ALS Research Laboratory.
Copyright:
Copyright 2015 Elsevier B.V., All rights reserved.
PY - 1990/6
Y1 - 1990/6
N2 - Rat skeletal muscle contains a 22 kd polypeptide that increases the level of choline acetyltransferase (ChAT) activity in cultures of embryonic rat spinal cord neurons and has been purified to homogeneity. The application of this factor, ChAT development factor or CDF, to developing chick embryos during the period of naturally occurring motoneuron cell death significantly increased the survival of motoneurons but did not affect the survival of dorsal root ganglion neurons or sympathetic preganglionic neurons (column of Terni). These results provide the first demonstration that an isolated, skeletal muscle-derived molecule can selectively enhance the survival of motoneurons in vivo and suggest that CDF may function in vivo to regulate the survival and development of motoneurons.
AB - Rat skeletal muscle contains a 22 kd polypeptide that increases the level of choline acetyltransferase (ChAT) activity in cultures of embryonic rat spinal cord neurons and has been purified to homogeneity. The application of this factor, ChAT development factor or CDF, to developing chick embryos during the period of naturally occurring motoneuron cell death significantly increased the survival of motoneurons but did not affect the survival of dorsal root ganglion neurons or sympathetic preganglionic neurons (column of Terni). These results provide the first demonstration that an isolated, skeletal muscle-derived molecule can selectively enhance the survival of motoneurons in vivo and suggest that CDF may function in vivo to regulate the survival and development of motoneurons.
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U2 - 10.1016/0896-6273(90)90142-3
DO - 10.1016/0896-6273(90)90142-3
M3 - Article
C2 - 2361012
AN - SCOPUS:0025282337
VL - 4
SP - 891
EP - 898
JO - Neuron
JF - Neuron
SN - 0896-6273
IS - 6
ER -