Evidence for insulin-like growth factor-I regulation of chick aortic elastogenesis.

The potential role of insulin-like growth factor-I (IGF-I) as a modulator of chick aortic embryogenesis was examined. Studies were designed to investigate the in vivo relationships between embryonic IGF-I serum concentrations, liver and aortic IGF-I mRNA steady-state levels and the inception and perpetuation of aortic elastogenesis. In addition to aortic tissue, elastogenesis was measured in heart and lung tissues in order to compare the responses of functionally unique elastin-containing tissues to the developmental appearance of IGF-I in embryonic serum. Our results demonstrate that the induction of aortic tropoelastin mRNA steady-state levels coincides with a major increase in serum IGF-I concentration. This is not the case with either lung or heart elastogenic responses. All three tissues examined (aorta, lung, and heart) exhibited different developmental patterns of tropoelastin mRNA steady-state levels during the embryonic ages studied (8- through 10-day). Only aortic tropoelastin mRNA levels paralleled the rise and fall of IGF-I serum levels. Steady-state levels of liver IGF-I mRNA peaked one day (9-day) prior to detectable IGF-I serum levels but otherwise mirrored the gradual, but steady decrease in IGF-I serum levels through 16-day. Aortic tissue also expresses IGF-I mRNA beginning at 8-day and continuing throughout the embryonic ages examined (16-day). Although the relative levels of aortic IGF-I mRNA are very low in comparison to corresponding mRNA levels in liver, the fact that IGF-I mRNA is transcribed in the aorta points to the possibility that autocrine and/or paracrine mechanisms of IGF-I action may be operative in aortic elastogenesis.