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BOR - Papers in Press, published online ahead of print October 29, 2003.
Biol Reprod 2003, 10.1095/biolreprod.103.022590
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Submitted August 25, 2003
Returned for revision September 12, 2003
Accepted October 21, 2003

Testis


Development of Leydig Cells in the Insulin-Like Growth Factor-1 (IGF-1) Knockout Mouse: Effects of IGF-1 Replacement and Gonadotropic Stimulation

Guimin Wang and Matthew P. Hardy *

* To whom correspondence should be addressed. E-mail: hardy{at}popcbr.rockefeller.edu.

Abstract
Targeted gene deletion of IGF-1 results in diminished numbers of Leydig cells (LCs) and lower circulating testosterone (T) levels in adult males. The impact of endogenous IGF-1 withdrawal on proliferation (labeling index, LI) and differentiation of LCs was investigated, testing for restorative effects of IGF-1 replacement and/or luteinizing hormone (LH) stimulation. With IGF-1 replacement in mutant mice, LIs increased more than 200% (P<0.05). LC numbers were also increased by 200%, whereas the numbers of intermediate cell progenitors (PLCs) were unchanged compared to mutant vehicle controls. LIs of PLCs in wildtype males increased by 200% after LH stimulation, and LC numbers were increased by 50% compared to vehicle-treated controls (P<0.05). In contrast, there was no effect of LH on LI in mutant mice, but LC numbers still increased by 30% (P<0.05). Additive effects on LI and cell numbers were observed in response to IGF-1 plus LH in mutants, implying that the two hormones use separate signaling pathways. Serum T and LH levels in wildtype and mutant males were equivalent. Exogenous LH increased T production by 8 fold in wildtype males (P<0.01). In mutant mice, neither LH stimulation nor IGF-1 alone affected serum T levels but, when added together, serum T increased by 2 fold (P<0.05). These data support the conclusion that: 1) IGF-1 is a critical autocrine and/or paracrine factor in the control of adult Leydig cell numbers and function; 2) LH is not a direct mitogenic factor for Leydig cells, and acts in part through IGF-1 to stimulate proliferative activity.

Key words: Insulin-like growth factor receptor • Leydig cells • Luteinizing hormone • Puberty • Testosterone


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