CAMP AND BFGF NEGATIVELY REGULATE TROPOMYOSIN EXPRESSION IN RAT CULTURED ASTROBLASTS

We have examined the expression of tropomyosin (TM) messenger RNAs (mR NAs) and protein isoforms in primary cultures of rat astroblasts durin g morphological changes. Three messenger RNA bands of 2.5, 1.8 and 1.2 kilobase pairs (kb) were detected by Northern blot. Using an antibody cross-reacting with all tropomyosin isoforms, we found that rat cereb ellar neonatal astroblasts expressed three tropomyosin protein isoform s termed TM-As1, TM-As2 and TM-As3 (As for Astroblast) with respective molecular masses of 38,000, 33,000 and 31,000. Treatment of cells wit h agents which promote or mimick the action of cyclic AMP, or with gro wth factors, is known to induce astroblast morphological alteration fr om flat, polygonal epitheloid cells into star-shaped, process-bearing cells. In the presence of dibutyryl cAMP (dBcAMP), forskolin or basic fibroblast growth factor (bFGF), these morphological changes were foun d to be associated with dramatic decreases of the three mRNA transcrip ts and also of the three protein isoforms. This decrease was reversed upon removal of the drugs. The pattern of the tropomyosin protein isof orms in cultured astroblasts showed that TM-As1, the most immunoreacti ve isoform recovered in the cytoskeletal insoluble cell fraction, had a developmental profile similar to that of F-actin. Therefore this iso form, which belongs to the high-molecular-mass family of proteins know n to interact strongly with F-actin, could specifically be involved in the regulation/control of F-actin stability and thus be associated wi th the plasticity of astroblasts.