Role of CREB in the regulatory action of sarsasapogenin on muscarinic M 1  receptor density during cell aging | Zendy

Hu Haiyan | Zendy; Zhang Rui | Zendy; Zhang Yongfang | Zendy; Xia Zongqin | Zendy; Hu Yaer | Zendy

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Role of CREB in the regulatory action of sarsasapogenin on muscarinic M 1 receptor density during cell aging

Author(s) -

Hu Haiyan,

Zhang Rui,

Zhang Yongfang,

Xia Zongqin,

Hu Yaer

Publication year - 2010

Publication title -

febs letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.593

H-Index - 257

eISSN - 1873-3468

pISSN - 0014-5793

DOI - 10.1016/j.febslet.2010.03.006

Subject(s) - creb , receptor , muscarinic acetylcholine receptor , muscarinic acetylcholine receptor m3 , transfection , muscarinic acetylcholine receptor m5 , chemistry , microbiology and biotechnology , endocrinology , biology , medicine , gene , biochemistry , transcription factor

This work studied the role of cyclic AMP responsive element binding protein (CREB) in the up‐regulation of M 1 muscarinic acetylcholine receptor (M 1 receptor) density by sarsasapogenin (ZMS) in CHO cells transfected with M 1 receptor gene (CHOm1 cells). During cell aging, sarsasapogenin elevated M 1 receptor density as well as CREB and phosphor‐CREB (pCREB) levels. CREB peaked earliest, followed by pCREB and M 1 receptor density peaked last. When CREB synthesis was blocked by antisense oligonucleotides, the elevation effect of sarsasapogenin on M 1 receptor density was abolished. These results suggest that sarsasapogenin up‐regulates M 1 receptor density in aged cells by promoting CREB production and phosphorylation. Furthermore, the results support the hypothesis that pCREB regulates M 1 receptor gene expression through heterodimer formation.

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