Balloon denudation of rat aorta induced IGF-I mRNA expression, peaking at about ninefold control levels 7 days after injury.
IGF-I may act as an important autocrine or paracrine regulator of smooth muscle cell proliferation in response to arterial wall injury.
Effect estimate: ninefold induction
Insulin-like growth factor I (IGF-I) is a widely distributed mitogen that mediates the growth-promoting effects of platelet-derived growth factor in mesenchymal cells. We show that rat aortic IGF-I messenger RNA (mRNA) is induced 24 hours after deendothelialization, at a time when smooth muscle cell proliferation within the intima is still not apparent. After 7 days, IGF-I mRNA induction peaks at about ninefold control levels and then falls to about threefold 14 days after denudation when smooth muscle cell proliferation is at its peak. We also show that, of the 5' untranslated IGF-I mRNA transcripts, only the class C transcript is expressed and regulated in aortic tissue. In contrast, treatment of rats with supraphysiological doses of growth hormone, the major endocrine regulator of IGF-I gene expression, elicited only twofold induction of aortic IGF-I mRNA. Our findings suggest that IGF-I may be an important autocrine or paracrine regulator of smooth muscle cell proliferation and that it may be significant in determining the cellular response to arterial wall injury.
Cercek et al. (Fri,) conducted a other in Arterial wall injury. Balloon denudation (deendothelialization) vs. Control levels (uninjured) was evaluated on IGF-I mRNA induction (ninefold induction). Balloon denudation of rat aorta induced IGF-I mRNA expression, peaking at about ninefold control levels 7 days after injury.