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Regulation of relaxin 3 gene expression via cAMP-PKA in a neuroblastoma cell line

✍ Scribed by Masaki Tanaka; Yoshihisa Watanabe; Kanji Yoshimoto

Publisher
John Wiley and Sons
Year
2009
Tongue
English
Weight
815 KB
Volume
87
Category
Article
ISSN
0360-4012

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✦ Synopsis

Abstract

Relaxin 3 is expressed in neurons of the brain stem that inneravate wide areas of the forebrain. Relaxin 3 mRNA levels in these neurons are increased in response to restraint stress, and by central administration of corticotropin‐releasing factor (CRF). In the present study, we observed that relaxin 3 was expressed in a mouse neuroblastoma cell line, Neuro2a, and investigated the intracellular signaling that activated relaxin 3 gene transcription in vitro. By means of a clone stably transfected with a relaxin 3 promoter‐EGFP gene, we observed that dibutyryl cyclic AMP and forskolin increased the relaxin 3 promoter activity. These increases were inhibited by pretreatment with PKA inhibitors, H89 and KT5720. Moreover, the promoter activity was enhanced by CRF treatment after expression of CRF‐R1 receptor on the cells. Taken together, these results indicate that relaxin 3 transcription is activated via the cAMP‐PKA pathway in the downstream of CRF‐R1. © 2008 Wiley‐Liss, Inc.

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