作者
Jacob Tfelt-Hansen, R John MacLeod, Naibedya Chattopadhyay, Shozo Yano, Steve Quinn, X Ren, Ernst F Terwilliger, Peter Schwarz, Edward M Brown
发表日期
2003/8
期刊
American Journal of Physiology-Endocrinology and Metabolism
卷号
285
期号
2
页码范围
E329-E337
出版商
American Physiological Society
简介
Elevated extracellular calcium ([Ca2+]o) and other agonists potentially acting via the calcium-sensing receptor (CaR) increase parathyroid hormone-related peptide (PTHrP) release from H-500 Leydig cells. Here, we provide strong evidence for the CaR's involvement by using a dominant negative CaR that attenuates high [Ca2+]o-induced PTHrP release. This effect is likely transcriptional, because high [Ca2+]o upregulates the PTHrP transcript, an effect that is abolished by actinomycin D. Regulation of PTHrP release by the CaR involves activation of PKC as well as ERK1/2, p38 MAPK, and JNK pathways. However, we show for the first time that high [Ca2+]o-induced activation of the stress-activated protein kinase SEK1 is PKC independent, because there is an additive effect of a PKC inhibitor in combination with the JNK inhibitor on [Ca2+]o-stimulated PTHrP release. Furthermore, high [Ca2+]o, in a PKC …
引用总数
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