October 9 - 12, 2012
Building 10 & Natcher Conference Center
- General Schedule of Events
- Opening Plenary Session
- Concurrent Symposia Sessions
- Poster Sessions
- National Graduate Student Research Conference
- FARE Award Ceremony
- Special Exhibits on Resources for Intramural Research
- TSA Research Festival Exhibit Show
- Clinical Center Tours
- Research Festival Committees
- Past Research Festivals
Thyroid hormone-mediated adrenal regression/remodeling
| Friday, November 08, 2013 — Poster Session IV | |||
|---|---|---|---|
2:00 p.m. – 4:00 p.m. |
FAES Academic Center (Upper-Level Terrace) |
NIDDK |
DEVBIO-4 |
Authors
- J. Huang
- D. Forrest
Abstract
At embryonic stages, the fetal adrenal cortex already has the ability to synthesize and secrete steroid hormones that are critical for fetal development. These functional fetal cortical cells then undergo regression and are replaced by continuously renewing adult-like cortical cells after birth. The continuously renewing adult cortical cells grow from the most outer layer of the cortex and form the “adult zone”, whereas fetal cortical cells stay in the inner portion of the cortex and form the “fetal zone”. During development, the fetal zone regresses while the adult zone grows. However, the mechanisms that regulate the differential development and the regression of the adrenal cortex remain unclear. Here, we first report that thyroid hormone signaling is active in the adrenal cortex, especially in the adrenal fetal zone. Thyroid hormone receptor, TRb1, and two thyroid hormone transporters, Mct8 and Mct10, specifically express in the fetal zone and are responsible for the thyroid hormone-mediated fetal zone hypertrophy. Our results point to the novel role of thyroid hormone in adrenal regression/remodeling. This study helps in the understanding of the mechanism that controls the cell fate of adrenal cortical cells and could further provide novel therapeutic interventions for adrenal cancer and adrenal insufficiency.
