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The Journal of Neuroscience, April 6, 2005, 25(14):3692-3700; doi:10.1523/JNEUROSCI.5225-04.2005

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Cellular/Molecular
Impeded Interaction between Schwann Cells and Axons in the Absence of Laminin 4

Wilhelm Wallquist,¹ Stefan Plantman,¹ Sebastian Thams,¹ Jill Thyboll,² Jarkko Kortesmaa,² Jan Lännergren,³ Anna Domogatskaya,² Sven Ove Ögren,¹ Mårten Risling,^1,4 Henrik Hammarberg,^1,5 Karl Tryggvason,² and Staffan Cullheim¹

Departments of ¹Neuroscience, ²Medical Biochemistry and Biophysics, and ³Physiology and Pharmacology, Karolinska Institute, 171 77 Stockholm, Sweden, ⁴Department of Defense Medicine, Swedish Defense Research Agency, 171 77 Stockholm, Sweden, and ⁵Department of Hand Surgery, Stockholm Söder Hospital, 118 87 Stockholm, Sweden

The Schwann cell basal lamina (BL) is required for normal myelination. Loss or mutations of BL constituents, such as laminin-2 (211), lead to severe neuropathic diseases affecting peripheral nerves. The function of the second known laminin present in Schwann cell BL, laminin-8 (411), is so far unknown. Here we show that absence of the laminin 4 chain, which distinguishes laminin-8 from laminin-2, leads to a disturbance in radial sorting, impaired myelination, and signs of ataxia and proprioceptive disturbances, whereas the axonal regenerative capacity is not influenced. In vitro studies show poor axon growth of spinal motoneurons on laminin-8, whereas it is extensive on laminin-2. Schwann cells, however, extend longer processes on laminin-8 than on laminin-2, and, in contrast to the interaction with laminin-2, solely use the integrin receptor 61 in their interaction with laminin-8. Thus, laminin-2 and laminin-8 have different critical functions in peripheral nerves, mediated by different integrin receptors.

Key words: myelin; extracellular matrix; Schwann cells; electron microscopy; neuropathy; regeneration

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Received July 22, 2004; revised February 21, 2005; accepted February 22, 2005.

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