Effects of insulin and IGF1 on SMCs

More than a decade ago different publications showed that insulin stimulates SMC proliferation in vitro (Stout 1990). We have observed that in non-cultured cells, SMCs directly taken from the human artery, insulin stimulates collagen secretion. This effect was probably produced by activation of the IGF1 receptors, because addition of insulin receptor-blocking antibodies did not show any inhibition. On the contrary, antibodies blocking IGF1 receptors inhibited the insulin-induced collagen secretion. We concluded that insulin is able to change the SMC phenotype by acting as a growth factor (Ruiz-Torres et al 1998).

Moreover, insulin stimulates the chemotaxis of SMCs directly dispersed from the human artery (Muñoz et al 1998). In these experiments this migration could be inhibited by insulin receptor-blocking antibodies, so we assumed that insulin was acting here through its specific receptors. Nevertheless, these results point out a very close relationship between the stimulating effect of insulin on both collagen secretion and migration, in spite of apparently acting through different types of receptor. Further experiments were required to clarify how insulin stimulates SMC migration.

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