Fibronectin expression in the normal and hypertrophic rat heart.

We examined changes in the expression of fibronectin during the induction of cardiac hypertrophy by L-triiodothyronine ad- ministration and by mineralocorticoidand salt-induced experi- mental hypertension. By use of Northern and Western blotting procedures, fibronectin was localized mainly in the atria of nor- mal rat hearts. Atria contained 10-and 5-fold higher relative concentrations of fibronectin mRNA and protein, respectively, compared with ventricles. During the progression of cardiac hypertrophy induced by L-triiodothyronine over a 10-d period, there was a progressive increase in fibronectin mRNA for the first 6 d followed by a return to control levels. The major change could be accounted for by changes in ventricular mRNA, which increased about four-to sixfold. In contrast, protein levels in ventricles increased progressively over the 10-d treatment pe- riod. Ribonuclease protection analysis indicated that the rela- tive amounts of fibronectin isoforms containing exons desig- nated EIIIA and EIIIB increased during the progression of hy- pertropy. When cardiac hypertrophy was induced by mineralocorticoid and salt treatment, increases in ventricular fibronectin mRNA and protein and the induction of alterna- tively spliced forms of fibronectin were also observed. How- ever, the extent and temporal pattern of fibronectin expression differed between the two experimental models. (J. Clin. Invest. 1992.89:392-401.) Key words: triiodothyronine * extracellular matrix * alternate splicing. hypertension * myocytes We found that fibronectin expression increased in both experimental models, but temporal and spatial differences in amounts of steady-state mRNA, alternatively spliced isoforms, and protein were observed between the two models.