Fibronectin (FN) is a dimeric glycoprotein found in the extracellular
matrix (ECM) of most tissues and serves as a bridge between cells and
the interstitial collagen meshwork. It also influences diverse process
es including cell growth, adhesion, migration, and wound repair. Multi
ple FN forms arise by the alternative splicing of a primary transcript
originating from a single gene. The spatial and temporal alterations
in FN expression in the cardiovascular system have been studied in vit
ro in cell culture and in vivo during fetal development, hypertrophy,
infarction, arterial injury and aging. This review describes character
istics of FN expression in cardiovascular system: 1. the FN phenotype
is regulated during development. A high FN mRNA level is related to an
early cardiac organogenesis and a progressive decrease that begins at
the fetal stage and continues through senescence. During cardiac onto
geny, there is a linear correlation between total FN mRNA accumulation
and the relative amounts of FN-EIIIA and EIIIB RNA. This correlation
is absent during cardiac growth in the adult. 2. A differential reexpr
ession of the FN isoforms is observed in both myocardium and aorta in
different models of hypertension or infarction but with different thre
shold and time course. Changes in total FN mRNA levels in hypertensive
models vary depending on the authors. Nevertheless the differences in
the expression of the fetal forms of FN mRNA observed among the vario
us models of hypertension-induced hypertrophy indicate that the proces
s of FN pre-mRNA splicing in the adult myocardium is specifically regu
lated and depends on the pathological situations and the type of cell.
Although the mechanisms of regulation are poorly understood their imp
ortance cannot be underestimated since they control cell phenotype and
behavior. Some possible mechanisms of regulation of the expression of
fibronectin within the myocardium are proposed using more advanced st
udies performed in other tissues and with other experimental models.