Current Biology
Volume 9, Issue 21, 4 November 1999, Pages 1251-1254, S1
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Integrins mediate a neuronal survival signal for oligodendrocytes

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Abstract

Target-dependent survival of newly differentiated cells is an important part of neural development. In the case of myelin-forming oligodendrocytes, it matches the number of oligodendrocytes to the available axons [1]. In addition to growth factors, an axonal signal regulates this survival: when axons are transected, oligodendrocytes die and, conversely, when the number of axons is increased by genetic manipulation, oligodendrocyte numbers increase [2], [3]. Newly formed oligodendrocytes that fail to contact axons undergo apoptosis, and co-culture experiments that model axon–glial interactions in vitro reveal a neuronal survival effect not present in neuron-conditioned medium [4], [5], suggesting that the signal is non-diffusible and present on the surface of axons. The nature of these neuronal signals is unknown, as are the mechanisms by which they interact with growth-factor-mediated survival signals. As integrins can regulate survival in other cell types [6], [7], [8], we determined whether integrins are involved in the neuronal survival effect. We found that the laminin receptor α6β1 integrin, which is expressed on oligodendrocytes, enhances the sensitivity of oligodendrocytes to the survival effect of growth factors. On the basis of this interaction between integrin and growth-factor-mediated signalling, we propose a simple model by which signals from axons and other cell types might interact to regulate oligodendrocyte cell numbers.

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EE Frost and R Milner, Wellcome/CRC Institute of Developmental Biology and Cancer, Tennis Court Road, Cambridge CB2 1QR, UK, and Department of Medical Genetics, University of Cambridge.

PC Buttery, Wellcome/CRC Institute of Developmental Biology and Cancer, Tennis Court Road, CB2 1QR, UK, and Department of Medical Genetics, University of Cambridge and Department of Neurology, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK.

C ffrench-Constant, Wellcome/CRC Institute of Developmental Biology and Cancer, Tennis Court Road, CB2 1QR, UK, and Department of Medical Genetics, University of Cambridge and Cambridge Centre for Brain Repair, University Forvie Site, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK.

Present address for EE Frost: Department of Anatomy and Cell Biology, Uniformed Services University, 4301 Jones Bridge Road, Bethesda, Maryland 20814, USA.

E-mail address for C ffrench-Constant (corresponding author): [email protected].