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Biochem Biophys Res Commun. 2007 Oct 12;362(1):11-16. doi: 10.1016/j.bbrc.2007.07.177. Epub 2007 Aug 9.

Activation of calcium-sensing receptor accelerates apoptosis in hyperplastic parathyroid cells.

Author information

1
Department of Nephrology, School of Medicine, Showa University, Tokyo, Japan.
2
Department of Internal Medicine, Showa University Northern Yokohama Hospital, 35-1, Chigasaki-chuo, Tsuzuki, Yokohama 224-8503, Japan. Electronic address: ogatah@med.showa-u.ac.jp.
3
First Department of Pathology, Wakayama Medical University, Wakayama, Japan.
4
Division of Nephrology and Blood Purification Medicine, Wakayama Medical University, Wakayama, Japan.
5
Division of Nephrology, Department of Internal Medicine, Showa University Fujigaoka Hospital, Yokohama, Japan.
6
Department of Internal Medicine, Showa University Northern Yokohama Hospital, 35-1, Chigasaki-chuo, Tsuzuki, Yokohama 224-8503, Japan.

Abstract

Calcimimetic compounds inhibit not only parathyroid hormone (PTH) synthesis and secretion, but also parathyroid cell proliferation. The aim of this investigation is to examine the effect of the calcimimetic compound NPS R-568 (R-568) on parathyroid cell death in uremic rats. Hyperplastic parathyroid glands were obtained from uremic rats (subtotal nephrectomy and high-phosphorus diet), and incubated in the media only or the media which contained high concentration of R-568 (10(-4)M), or 10% cyclodextrin, for 6h. R-568 treatment significantly suppressed medium PTH concentration compared with that of the other two groups. R-568 treatment not only increased the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay-positive cells, but also induced the morphologic changes of cell death determined by light or electron microscopy. These results suggest that CaR activation by R-568 accelerates parathyroid cell death, probably through an apoptotic mechanism in uremic rats in vitro.

PMID:
17706605
DOI:
10.1016/j.bbrc.2007.07.177
[Indexed for MEDLINE]

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