Insulin-like growth factor 1 is required for G 2 progression in the estradiol-induced mitotic cycle

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Abstract
Insulin-like growth factor 1 (IGF1) has been proposed as a “G 1 -progression factor” and as a mediator of estradiol’s (E2) mitogenic effects on the uterus. To test these hypotheses, we compared E2’s mitogenic effects on the uteri of Igf1 -targeted gene deletion (null) and wild-type littermate mice. The proportion of uterine cells involved in the cell cycle and G 1 - and S-phase kinetics were not significantly different in wild-type and Igf1 -null mice. However, the appearance of E2-induced mitotic figures and cell number increases were profoundly retarded in Igf1 -null uterine tissue. There was a significant increase in nuclear DNA concentration in Igf1 -null cells, consistent with a G 2 arrest. Interestingly, apoptotic cells were also significantly reduced in abundance, and the normal massive apoptotic response to E2 withdrawal was absent in the Igf1 -null uterus. These data show that Igf1 is an essential mediator of E2’s mitogenic effects, with a critical role not in G 1 progression but in G 2 progression.

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