ASTROCYTES AND NEURONS REGULATE THE EXPRESSION OF THE NEURAL RECOGNITION MOLECULE JANUSIN BY CULTURED OLIGODENDROCYTES

Janusin (formerly designated J1-160/180) is an extracellular matrix gl ycoprotein highly homologous to tenascin, consisting of two major mole cular forms of 160 and 180 kD expressed by oligodendrocytes and in mye lin. Janusin expression is upregulated during myelination and in the a dult it remains expressed at lower levels. It is also present at the n ode of Ranvier, where myelin, axon, and astrocytic process are in clos e contact. To gain an understanding of the regulatory mechanisms which may underlie expression of janusin, the differentiation stage-depende nt expression of janusin was studied in cultures enriched in mouse oli godendrocytes and their precursor cells. Expression of janusin by thes e cells was highest on both A2B5(+) and O4(+)/O1(-) oligodendroglial p recursor cells and a subset of myelin associated glycoprotein-positive ((MAG(+))) oligodendrocytes. Hardly any of the more differentiated O1 (+) or O10(+) oligodendrocytes expressed janusin. Expression of janusi n was influenced by co-culture with astrocytes or neurons. Astrocytes or astrocytic-conditioned culture supernatants elevated the expression of janusin by the more differentiated oligodendrocytes (O1(+) or MAG( +) cells), while its expression by oligodendroglial precursor cells wa s relatively unchanged. Platelet-derived growth factor, but not basic fibroblast growth factor, also elevated the expression of janusin by O 1(+) or O10(+) oligodendrocytes. In contrast, co-culture with neurons originating from dorsal root ganglia or spinal cord decreased the expr ession of cell-bound janusin by oligodendrocytes and their precursor c ells. These observations indicate that expression of janusin on these cells in culture is susceptible to opposing regulatory influences from astrocytes and neurons. Such influences may modulate the temporal and spatial distribution of janusin in the developing and adult central n ervous system. (C) 1993 Wiley-Liss, Inc.