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ID 20100
本文ファイル
著者
Yoshida, Eri
Tsutsumi, Shinichi
Kuruta, Yoshihiro
Kato, Yukio
キーワード
PTH
PTHrP
RA
Ihh
chondrocyte
growth plate
抄録(英)
Indian hedgehog (Ihh) is highly expressed in prehypertrophic chondrocytes in vivo and has been proposed to regulate the proliferation and maturation of chondrocytes and bone collar formation in the growth plate. In high-density cultures of rabbit growth-plate chondrocytes, Ihh mRNA was also expressed at the highest level in the prehypertrophic stage. To explore endogenous factors that regulate Ihh expression in chondrocytes, we examined the effects of various growth factors on Ihh mRNA expression in this system. Retinoic acid (RA) and bone morphogenetic protein-2 enhanced Ihh mRNA expression, whereas PTH/PTH-related peptide (PTHrP) markedly suppressed Ihh expression. RA at more than 10-8 M induced the expression of Ihh and Patched 1 (Ptc1) within 3 h, before it increased the type X collagen mRNA level at 6–24 h. Cycloheximide blocked the up-regulation of Ihh by RA, indicating the requirement of de novo protein synthesis for this stimulation. These findings suggest that RA is involved in the up-regulation of Ihh during endochondral bone formation. In contrast to RA, PTH (1–84) at 10-7 M abolished the mRNA expression of Ihh and Ptc1 within 2–4 h, before it suppressed the expression of type X collagen at 12–24 h. The inhibition of Ihh expression by PTH (1–84) did not require de novo protein synthesis. PTH (1–34), PTHrP (1–34), and (Bu)2cAMP also suppressed Ihh expression. On the other hand, Ihh has been reported to induce PTHrP synthesis in the perichondrium. Consequently, the direct inhibitory action of PTH/PTHrP on Ihh appears to be a negative feedback mechanism that prevents excess PTHrP accumulation in cartilage.
掲載誌名
Experimental Cell Research
265巻
1号
開始ページ
64
終了ページ
72
出版年月日
2001-04-15
出版者
Elsevier
ISSN
0014-4827
NCID
出版者DOI
PubMedID
言語
英語
NII資源タイプ
学術雑誌論文
広大資料タイプ
学術雑誌論文
DCMIタイプ
text
フォーマット
application/pdf
著者版フラグ
author
権利情報
Copyright (c) 2001 Academic Press.
関連情報URL
部局名
医歯薬学総合研究科