ACTIN ISOFORM AND ALPHA(1B)-ADRENOCEPTOR GENE-EXPRESSION IN AORTIC AND CORONARY SMOOTH-MUSCLE IS INFLUENCED BY CYCLICAL STRETCH

The occurrence of vascular domains with specific biological and pharma cological characteristics suggests that smooth muscle cells in differe nt arteries may respond differentially to a wide range of environmenta l stimuli. To determine if some of these vessel-specific differences m ay be attributable to mechano-sensitive gene regulation, the influence of cyclical stretch on the expression of actin isoform and alpha(1B)- adrenoceptor genes was examined in aortic and coronary smooth muscle c ells. Cells were seeded on an elastin substrate and subjected to maxim al stretching (24% elongation) and relaxation cycles at a frequency of 120 cycles/min in a Flexercell strain unit for 72 h. Total RNA was ex tracted and hybridized to radiolabeled cDNA probes to assess gene expr ession. Stretch caused a greater reduction of actin isoform mRNA level s in aortic smooth muscle cells as compared to cells from the coronary artery. Steady-state mRNA levels of alpha(1B)-adrenoceptor were also decreased by cyclical stretch in both cell types but the magnitude of the response was greater in coronary smooth muscle cells. No changes i n alpha(1B)-adrenoceptor or beta/gamma-actin steady-state mRNA levels were observed in H4IIE cells, a nonvascular, immortalized cell line, T he relative gene expression of heat shock protein 70 was not influence d by the cyclic stretch regimen in any of these cell types. These resu lts suggest that stretch may participate in the regulation of gene exp ression in vascular smooth muscle cells and that this response exhibit s some degree of cell-specificity.