Angiotensin II regulates tenascin gene expression in vascular smooth muscle cells.

摘要: Angiotensin II, a vasoactive peptide, has been implicated in the pathophysiology of number vascular wall abnormalities. Since aberrant extracellular matrix deposition contributes to pathogenesis vessel disease, we examined potential involvement angiotensin II regulation synthesis by smooth muscle cells. Immunoprecipitation newly synthesized proteins showed that, under serum-free conditions, cultured cells constitutively produced high levels fibronectin, small amounts laminin, and barely detectable amount tenascin. treatment increased 230-kDa tenascin glycoprotein 9-fold fibronectin only 30-40% during 24-h period, without stimulating laminin production or general increase secreted proteins. Concomitant with saralasin, competitive inhibitor prevented stimulation observed II. The immunoprecipitable was preceded an mRNA. Levels transcripts (8.4 7.0 kilobase) were significantly within 2 h after treatment, reached maximum (10- 12-fold) 4 h, remained elevated 18 h. induction completely blocked actinomycin D. Serum also induced mRNA, but different time course. mRNA evident at maximal declined control 8 These results indicate that exerts rapid selective biosynthesis, least part transcriptional level. This suggests may alter composition antiadhesive protein