Prenatal flutamide enhances survival in a myogenic mouse model of spinal bulbar muscular atrophy.

ABSTRACT:

Background

Spinal bulbar muscular atrophy (SBMA) is caused by a CAG repeat expansion mutation in the androgen receptor (AR) gene, and mutant AR is presumed to act in motoneurons to cause SBMA. However, we found that mice overexpressing wild-type (wt) AR solely in skeletal muscle fibers display the same androgen-dependent disease phenotype as when mutant AR is broadly expressed, challenging the assumptions that only an expanded AR can induce disease and that SBMA is strictly neurogenic. We have previously reported that AR toxicity was ligand dependent in our model, and that very few transgenic (tg) males survived beyond birth.

Methods

We tested whether the AR antagonist flutamide could block perinatal toxicity. tg males were treated prenatally with flutamide and assessed for

SUBMITTER: Johansen JA 

PROVIDER: S-EPMC3030474 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature