Abstract
AbstractWhereas the animal lectin galectin‐3 is only barely detectable in the adult sciatic nerve, its expression level is substantially upregulated in the damaged nerve (1). In the present study, we demonstrate that in the mouse, the expression of galectin‐3 increases during normal peripheral nerve development and is further potentiated in the adult sciatic nerve under conditions of in vitro degeneration. In cell cultures derived from neonatal sciatic nerve galectin‐3 is expressed by about 50% of L1‐positive Schwann cells. Comparable results were obtained for cultured late immature Schwann cells derived from hindlimbs of 17.5‐day‐old mouse embryos. In cell cultures derived from hindlimbs of 14‐day‐old embryos, by contrast, only about 5% of the L1‐positive early immature Schwann cells expressed galectin‐3. Our findings demonstrate that the upregulation of galectin‐3 expression by activated adult Schwann cells is not a part of a dedifferentiation program, but rather attributes to a phenotype specific for injury‐activated Schwann cells.
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