SAT-562 Thyroid Hormone Transporter Mct8 is Specially Expressed in the Adrenal Gland Inner Cortex and Partially Mediates the Thyroid Hormone Action in the Adrenal Cortex.

Abstract

It is well known that thyroid hormone plays a key role in amphibian metamorphosis and mammalian tissue remodeling. We and others have reported that treatment with thyroid hormone will prevent or postpone the regression of the adrenal inner cortex (X-zone) and leads to X-zone hypertrophy in mice. The expression of thyroid hormone receptor beta 1 (TRβ1) in the adrenal inner cortex indicates that thyroid hormone could elicit its function directly on this cell population. To support this idea, we examined the expression and the function of major thyroid hormone transporters Mct8, Mct10, and Oatp1c1 in mouse adrenal glands. RNA-seq data showed that the expression levels of Mct10 and Oatp1c1 are relatively low in the adrenal gland (with RPKM less than 5 and 1, respectively) whereas Mct8 is the most abundant transporter (with RPKM around 20). Quantitative RT-PCR showed that Mct8 in the adrenal gland has an expression profile similar to X-zone marker genes and TRβ1 throughout developmental stages. LacZ staining showed similarities between Mct8 and TRβ1 expression, with both specifically expressed in the most inner cortex of the adrenal gland next to the medulla. However, by using thyroid hormone (T3) treatment, we found that the T3-mediated effect in the adrenal gland was not fully blocked in Mct8 knock-out mice. The expression of thyroid hormone transporter Mct8 in the adrenal inner cortex supports our claim that transporters mediate the direct action of thyroid hormone in the adrenal inner cortex. The blunted response to thyroid hormone in Mct8 knockout mice suggests that Mct8 is responsible for the thyroid hormone action in the adrenal gland. However, the deletion of Mct8 does not completely block thyroid hormones effect in the adrenal gland. Our finding suggests other thyroid hormone transporter(s) in the adrenal gland are also responsible for thyroid hormone signaling in the adrenal gland.