Luo L G, Jackson I M
Division of Endocrinology, Rhode Island Hospital, Brown University School of Medicine, Providence 02903, USA.
Peptides. 1998;19(8):1295-302. doi: 10.1016/s0196-9781(98)00074-6.
The proto-oncogenes, cfos/cjun, are co-localized with thyrotropin-releasing hormone (TRH) in cultured anterior pituitary cells and increase following exposure to dexamethasone (Dex). To assess the role of cfos and cjun in the Dex stimulation of TRH gene expression, we used antisense oligonucleotides to block cfos and cjun expression in order to reduce formation of activating protein-1 (AP-1). The results showed that the antisense oligonucleotides together effectively reduced cfos/cjun gene expression and consequently the glucocorticoid stimulation of TRH peptide and mRNA. The findings indicate that cfos/cjun are involved in the glucocorticoid activation of TRH gene expression.
原癌基因cfos/cjun在培养的垂体前叶细胞中与促甲状腺激素释放激素(TRH)共定位,并且在暴露于地塞米松(Dex)后表达增加。为了评估cfos和cjun在地塞米松刺激TRH基因表达中的作用,我们使用反义寡核苷酸来阻断cfos和cjun的表达,以减少活化蛋白-1(AP-1)的形成。结果表明,反义寡核苷酸共同有效地降低了cfos/cjun基因的表达,从而减少了糖皮质激素对TRH肽和mRNA的刺激。这些发现表明cfos/cjun参与了糖皮质激素对TRH基因表达的激活。