| Literature DB >> 29969651 |
Justin R Welden1, Zhaiyi Zhang1, Marilyn J Duncan2, Marina Falaleeva1, Timothy Wells3, Stefan Stamm4.
Abstract
The serotonin receptor 2C (5HT2C) is an important drug target to treat obesity and depression. Its pre-mRNA undergoes alternative splicing, encoding a short RNA1 isoform that is localized intracellularly and a full-length isoform (RNA2) that can reach the cell membrane. These splicing isoforms are deregulated in Prader-Willi syndrome (PWS), due to the loss of a trans-acting regulatory RNA, SNORD115. Here we show that the 5HT2C mRNA is expressed in the posterior pituitary, suggesting that 5HT2C mRNA is generated in the hypothalamus and subsequently conveyed by axonal transport. In the pituitary, the ratio of 5HT2C isoforms is regulated by feeding, and can be manipulated using a splice-site changing oligonucleotide injected into the blood. The pituitary expression of the 5HT2C mRNA may constitute a previously unknown mechanism whereby serotonin in the circulation or drugs targeting the 5HT2C might induce side-effects. Finally, the deregulation of 5HT2C splicing isoforms in PWS could contribute to the known hormonal imbalances.Entities:
Keywords: Alternative splicing; Pituitary; Prader-Willi syndrome; Serotonin receptor 2C
Mesh:
Substances:
Year: 2018 PMID: 29969651 DOI: 10.1016/j.neulet.2018.06.051
Source DB: PubMed Journal: Neurosci Lett ISSN: 0304-3940 Impact factor: 3.046