期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 96, 期 3, 页码 632-640出版社
WILEY
DOI: 10.1002/jcb.20550
关键词
parathyroid hormone; amphiregulin; osteoblastic cells; protein kinase A; cAMP response element-binding protein (CREB)
资金
- NIDDK NIH HHS [DK48109] Funding Source: Medline
Parathyroid hormone (PTH), an anabolic agent for bone metabolism, has profound effects on gene expression in the osteoblast. Recently, we identified that amphiregulin (AR), an EGF-like ligand, is an immediate early gene for PTH treatment and has an important role in bone metabolism. In the present report, by using different PTH peptide fragments, protein kinase activators, and inhibitors, we have demonstrated that PTH regulates amphiregulin in a cAMP-protein kinase A (PKA)-dependent manner both in vitro and in vivo. We found that the phosphorylation of cAMP-response element (CRE)-binding protein (CREB) preceded AIR transcription after PTH treatment. Moreover, luciferase reporter assays revealed that the binding of phosphorylated CREB to a conserved CRE site in the AIR promoter plays an important role in basal, PTH-induced, and prostaglandin E-2 (PGE(2))-induced AIR expression in osteoblastic cells. In summary, our data suggest that PTH-induced AIR mRNA expression is mediated primarily through cAMP-PKA-CREB signaling.
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