Retinol-binding protein is produced by rabbit chondrocytes and responds to parathyroid hormone (PTH)/PTH-related peptide-cyclic adenosine monophosphate pathway
Retinol-binding protein is produced by rabbit chondrocytes and responds to parathyroid hormone (PTH)/PTH-related peptide-cyclic adenosine monophosphate pathway
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DOI：
10.1210/en.140.3.1075
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发表时间：
1999-03-01
期刊：
影响因子：
4.8
通讯作者：
Kato, Y
中科院分区：
文献类型：
--
作者：
Kawashima-Ohya, Y;Kurata, Y;Kato, Y
PTH和二丁基cAMP [(Bu)(2)cAMP]在兔生长板软骨细胞培养的条件培养基中诱导了一种19 kda蛋白的表达。经氨基末端序列分析和抗rep单克隆抗体免疫印迹分析，鉴定该蛋白为血浆视黄醇结合蛋白（RBP）。Northern blot分析显示，PTH、PTH相关肽（PTHrP）和（Bu）(2)cAMP增加了软骨细胞培养中REP信使RNA （mRNA）的水平。此外，PTH和（Bu）(2)cAMP在3 h和24 h分别显著诱导REP mRNA表达10倍和40倍，表明存在翻译前调控作用。在肝癌细胞中，PTH、PTHrP和（Bu）(2)cAMP诱导的mRNA表达水平与视黄酸（RA）一样高，视黄酸是一种强效的REP诱导剂。在软骨组织中也检测到REP mRNA的水平高于除肝脏外的其他组织。在培养基中加入REP和PTH/PTHrP均能抑制RA对生长板软骨细胞的去分化活性。这些结果表明，体内和体外软骨细胞都能合成和分泌REP，提示PTH/PTHrP通过软骨细胞中REP的产生调节RA的作用。
PTH and dibutyryl cAMP [(Bu)(2)cAMP] induced the expression of a 19-kDa protein in the conditioned media of rabbit growth plate chondrocyte cultures. The 19-kDa protein was identified as plasma retinol-binding protein (RBP) by aminoterminal sequence analysis and immunoblot analysis with an anti-REP monoclonal antibody. Northern blot analysis showed that PTH, PTH-related peptide (PTHrP), and (Bu)(2)cAMP increased the REP messenger RNA (mRNA) level in chondrocyte cultures. Further, both PTH and (Bu)(2)cAMP markedly induced the expression of REP mRNA by about 10-fold at 3 h and by about 40-fold at 24 h, indicating a pretranslational regulation. The level of the mRNA expression induced by PTH, PTHrP, and (Bu)(2)cAMP was as high as that by retinoic acid (RA), known as a potent inducer of REP in hepatoma cells. REP mRNA was also detected in cartilage tissues at higher levels than in the other tissues examined except liver. Both REP and PTH/PTHrP inhibited the dedifferentiative activity of RA on growth plate chondrocytes when added to the culture medium. These results demonstrate that chondrocytes synthesize and secrete REP in vivo and in vitro and suggest that PTH/PTHrP modulates the effect of RA by means of REP production in chondrocytes.