| First Author | Huang CC | Year | 2015 |
| Journal | Endocrinology | Volume | 156 |
| Issue | 6 | Pages | 2338-48 |
| PubMed ID | 25774556 | Mgi Jnum | J:222168 |
| Mgi Id | MGI:5644085 | Doi | 10.1210/en.2015-1118 |
| Citation | Huang CC, et al. (2015) A Novel Population of Inner Cortical Cells in the Adrenal Gland That Displays Sexually Dimorphic Expression of Thyroid Hormone Receptor-beta1. Endocrinology 156(6):2338-48 |
| abstractText | The development of the adrenal cortex involves the formation and then subsequent regression of immature or fetal inner cell layers as the mature steroidogenic outer layers expand. However, controls over this remodeling, especially in the immature inner layer, are incompletely understood. Here we identify an inner cortical cell population that expresses thyroid hormone receptor-beta1 (TRbeta1), one of two receptor isoforms encoded by the Thrb gene. Using mice with a Thrb(b1) reporter allele that expresses lacZ instead of TRbeta1, beta-galactosidase was detected in the inner cortex from early stages. Expression peaked at juvenile ages in an inner zone that included cells expressing 20-alpha-hydroxysteroid dehydrogenase, a marker of the transient, so-called X-zone in mice. The beta-galactosidase-positive zone displayed sexually dimorphic regression in males after approximately 4 weeks of age but persisted in females into adulthood in either nulliparous or parous states. T3 treatment promoted hypertrophy of inner cortical cells, induced some markers of mature cortical cells, and, in males, delayed the regression of the TRbeta1-positive zone, suggesting that TRbeta1 could partly divert the differentiation fate and counteract male-specific regression of inner zone cells. TRbeta1-deficient mice were resistant to these actions of T3, supporting a functional role for TRbeta1 in the inner cortex. |
