Transforming growth factors-beta 1 and beta 2 are mitogens for rat Schwann cells

doi:10.1083/jcb.109.6.3419

This Article

	Full Text (PDF, 1019K)
	Alert me when this article is cited
	Citation Map

Services

	Email this article
	Similar articles in this journal
	Similar articles in PubMed
	Alert me to new content in the JCB
	Download to citation manager

Citing Articles

	Citing Articles via HighWire
	Citing Articles via CrossRef
	Citing Articles via Google Scholar

Google Scholar

	Articles by Ridley, A. J.
	Articles by Land, H.
	Search for Related Content

PubMed

	PubMed Citation
	Articles by Ridley, A. J.
	Articles by Land, H.


Social Bookmarking

	What's this?

ARTICLES

Transforming growth factors-beta 1 and beta 2 are mitogens for rat Schwann cells

AJ Ridley, JB Davis, P Stroobant and H Land
Imperial Cancer Research Fund, London, United Kingdom.

Transforming growth factor-beta 1 (TGF-beta 1) and TGF-beta 2 were found to be potent mitogens for purified rat Schwann cells, each stimulating DNA synthesis in quiescent cells and also increasing their proliferation rate. Half-maximal stimulation of DNA synthesis occurred at approximately 0.1 ng/ml TGF-beta 1 or TGF-beta 2. Mitogenic stimulation by TGF-beta 1 and TGF-beta 2 was enhanced by forskolin, which activates adenylate cyclase, at concentrations up to 0.5 microM forskolin. However, at 5 microM forskolin, the synergistic interaction between forskolin and TGF-beta 1 was abolished. These results are in contrast to the observed synergy between forskolin and another Schwann cell mitogen, glial growth factor (GGF). Both 0.5 and 5 microM forskolin were found to enhance the stimulation of DNA synthesis by partially purified GGF (GGF-CM). As well as being functionally distinct, TGF-beta 1 and GGF-CM activities were also physically separable by chromatography on a Superose 12 gel permeation column. Thus, TGF-beta 1 and beta 2 are rat Schwann cell mitogens, and Schwann cells are one of the few normal cell populations to respond mitogenically to TGF-beta.
Add to CiteULike CiteULike Add to Complore Complore Add to Connotea Connotea Add to Del.icio.us Del.icio.us Add to Digg Digg Facebook Add to Reddit Reddit Add to Technorati Technorati Twitter What's this?

This article has been cited by other articles:

Jacob, C., Grabner, H., Atanasoski, S., Suter, U. (2008). Expression and localization of Ski determine cell type-specific TGF{beta} signaling effects on the cell cycle. JCB 182: 519-530 [Abstract] [Full Text]
Rasouli, A., Bhatia, N., Suryadevara, S., Cahill, K., Gupta, R. (2006). Transplantation of Preconditioned Schwann Cells in Peripheral Nerve Grafts After Contusion in the Adult Spinal Cord. Improvement of Recovery in a Rat Model. JBJS 88: 2400-2410 [Abstract] [Full Text]
D'Antonio, M., Droggiti, A., Feltri, M. L., Roes, J., Wrabetz, L., Mirsky, R., Jessen, K. R. (2006). TGFbeta Type II Receptor Signaling Controls Schwann Cell Death and Proliferation in Developing Nerves.. J. Neurosci. 26: 8417-8427 [Abstract] [Full Text]
Atanasoski, S., Scherer, S. S., Sirkowski, E., Leone, D., Garratt, A. N., Birchmeier, C., Suter, U. (2006). ErbB2 Signaling in Schwann Cells Is Mostly Dispensable for Maintenance of Myelinated Peripheral Nerves and Proliferation of Adult Schwann Cells after Injury. J. Neurosci. 26: 2124-2131 [Abstract] [Full Text]
Crawford, S. E., Stellmach, V., Ranalli, M., Huang, X., Huang, L., Volpert, O., De Vries, G. H., Abramson, L. P., Bouck, N. (2002). Pigment epithelium-derived factor (PEDF) in neuroblastoma: a multifunctional mediator of Schwann cell antitumor activity. J. Cell Sci. 114: 4421-4428 [Abstract] [Full Text]
Watanabe, T, Oda, Y, Tamiya, S, Masuda, K, Tsuneyoshi, M (2001). Malignant peripheral nerve sheath tumour arising within neurofibroma. An immunohistochemical analysis in the comparison between benign and malignant components. J. Clin. Pathol. 54: 631-636 [Abstract] [Full Text]
Tikoo, R., Zanazzi, G., Shiffman, D., Salzer, J., Chao, M. V. (2000). Cell Cycle Control of Schwann Cell Proliferation: Role of Cyclin-Dependent Kinase-2. J. Neurosci. 20: 4627-4634 [Abstract] [Full Text]
Bruno, E., Horrigan, S. K., Van Den Berg, D., Rozler, E., Fitting, P. R., Moss, S. T., Westbrook, C., Hoffman, R. (1998). The Smad5 Gene Is Involved in the Intracellular Signaling Pathways That Mediate the Inhibitory Effects of Transforming Growth Factor-beta on Human Hematopoiesis. Blood 91: 1917-1923 [Abstract] [Full Text]
Fleur, M. L., Underwood, J. L., Rappolee, D. A., Werb, Z. (1996). Basement Membrane and Repair of Injury to Peripheral Nerve: Defining a Potential Role for Macrophages, Matrix Metalloproteinases, and Tissue Inhibitor of Metalloproteinases-1. JEM 184: 2311-2326 [Abstract] [Full Text]
Lisak, R. P (1996). In vitro studies of glial cells: what can we learn about demyelinating diseases?. Mult Scler 2: 173-178 [Abstract]
Ambros, I. M., Zellner, A., Roald, B., Amann, G., Ladenstein, R., Printz, D., Gadner, H., Ambros, P. F. (1996). Role of Ploidy, Chromosome 1p, and Schwann Cells in the Maturation of Neuroblastoma. NEJM 334: 1505-1511 [Abstract] [Full Text]
McMurray, H., Proudfoot, D, Davis, J., Parrott, D., Bowyer, D. (1993). A small molecular mass inhibitor of growth of 3T3 cells and porcine aortic smooth muscle cells released from the macrophage cell line P388D1. J. Cell Sci. 106: 1301-1311 [Abstract]
Lefcort, F, Venstrom, K, McDonald, J., Reichardt, L. (1992). Regulation of expression of fibronectin and its receptor, alpha 5 beta 1, during development and regeneration of peripheral nerve. Development 116: 767-782 [Abstract]