QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, August 20, 2003, 23(20):7710-7718

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (37) Citing Articles via Google Scholar Google Scholar Articles by Mason, J. L. Articles by Goldman, J. E. Search for Related Content PubMed PubMed Citation Articles by Mason, J. L. Articles by Goldman, J. E.

 Previous Article  |  Next Article 

Insulin-Like Growth Factor (IGF) Signaling through Type 1 IGF Receptor Plays an Important Role in Remyelination

Jeffrey L. Mason,¹ Shouhong Xuan,² Ioannis Dragatsis,² Argiris Efstratiadis,² and James E. Goldman¹

¹Department of Pathology and The Center for Neurobiology and Behavior, and ²Department of Genetics and Development, Columbia University, New York, New York 10032

We examined the role of IGF signaling in the remyelination process by disrupting the gene encoding the type 1 IGF receptor (IGF1R) specifically in the mouse brain by Cre-mediated recombination and then exposing these mutants and normal siblings to cuprizone. This neurotoxicant induces a demyelinating lesion in the corpus callosum that is reversible on termination of the insult. Acute demyelination and oligodendrocyte depletion were the same in mutants and controls, but the mutants did not remyelinate adequately. We observed that oligodendrocyte progenitors did not accumulate, proliferate, or survive within the mutant mice, compared with wild type, indicating that signaling through the IGF1R plays a critical role in remyelination via effects on oligodendrocyte progenitors.

Key words: demyelination; oligodendrocyte; progenitors; apoptosis; macrophages; transgenic

---

Received Apr. 10, 2003; revised Jun. 11, 2003; accepted Jul. 7, 2003.

This article has been cited by other articles:

				T. W. Gould and H. Enomoto Neurotrophic Modulation of Motor Neuron Development Neuroscientist, February 1, 2009; 15(1): 105 - 116. [Abstract] [PDF]

				H. Schori, R. Shechter, I. Shachar, and M. Schwartz Genetic Manipulation of CD74 in Mouse Strains of Different Backgrounds Can Result in Opposite Responses to Central Nervous System Injury J. Immunol., January 1, 2007; 178(1): 163 - 171. [Abstract] [Full Text] [PDF]

				D. Linares, M. Taconis, P. Mana, M. Correcha, S. Fordham, M. Staykova, and D. O. Willenborg Neuronal Nitric Oxide Synthase Plays a Key Role in CNS Demyelination J. Neurosci., December 6, 2006; 26(49): 12672 - 12681. [Abstract] [Full Text] [PDF]

				B. Emery, H. S. Cate, M. Marriott, T. Merson, M. D. Binder, C. Snell, P. Y. Soo, S. Murray, B. Croker, J.-G. Zhang, et al. Suppressor of cytokine signaling 3 limits protection of leukemia inhibitory factor receptor signaling against central demyelination PNAS, May 16, 2006; 103(20): 7859 - 7864. [Abstract] [Full Text] [PDF]

				P. H. Larsen, A. G. DaSilva, K. Conant, and V. W. Yong Myelin formation during development of the CNS is delayed in matrix metalloproteinase-9 and -12 null mice. J. Neurosci., February 22, 2006; 26(8): 2207 - 2214. [Abstract] [Full Text] [PDF]

				B. B. Murinson, D. R. Archer, Y. Li, and J. W. Griffin Degeneration of Myelinated Efferent Fibers Prompts Mitosis in Remak Schwann Cells of Uninjured C-Fiber Afferents J. Neurosci., February 2, 2005; 25(5): 1179 - 1187. [Abstract] [Full Text] [PDF]

				W. H. Shen, J.-H. Zhou, S. R. Broussard, R. W. Johnson, R. Dantzer, and K. W. Kelley Tumor Necrosis Factor {alpha} Inhibits Insulin-Like Growth Factor I-Induced Hematopoietic Cell Survival and Proliferation Endocrinology, July 1, 2004; 145(7): 3101 - 3105. [Abstract] [Full Text] [PDF]

				J. L. Mason, A. Toews, J. D. Hostettler, P. Morell, K. Suzuki, J. E. Goldman, and G. K. Matsushima Oligodendrocytes and Progenitors Become Progressively Depleted within Chronically Demyelinated Lesions Am. J. Pathol., May 1, 2004; 164(5): 1673 - 1682. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help