| First Author | Chiappini F | Year | 2013 |
| Journal | Mol Cell Endocrinol | Volume | 365 |
| Issue | 1 | Pages | 84-94 |
| PubMed ID | 23000398 | Mgi Jnum | J:193787 |
| Mgi Id | MGI:5469556 | Doi | 10.1016/j.mce.2012.09.006 |
| Citation | Chiappini F, et al. (2013) Family members CREB and CREM control thyrotropin-releasing hormone (TRH) expression in the hypothalamus. Mol Cell Endocrinol 365(1):84-94 |
| abstractText | Thyrotropin-releasing hormone (TRH) in the paraventricular nucleus (PVN) of the hypothalamus is regulated by thyroid hormone (TH). cAMP response element binding protein (CREB) has also been postulated to regulate TRH expression but its interaction with TH signaling in vivo is not known. To evaluate the role of CREB in TRH regulation in vivo, we deleted CREB from PVN neurons to generate the CREB1(DeltaSIM1) mouse. As previously shown, loss of CREB was compensated for by an up-regulation of CREM in euthyroid CREB1(DeltaSIM1) mice but TSH, T(4) and T(3) levels were normal, even though TRH mRNA levels were elevated. Interestingly, TRH mRNA expression was also increased in the PVN of CREB1(DeltaSIM1) mice in the hypothyroid state but became normal when made hyperthyroid. Importantly, CREM levels were similar in CREB1(DeltaSIM1) mice regardless of thyroid status, demonstrating that the regulation of TRH by T(3)in vivo likely occurs independently of the CREB/CREM family. |
