前列腺素F(2α)对na依赖性磷酸盐在成骨细胞样细胞中的转运的刺激作用。

IF 3

Prostaglandins, leukotrienes, and essential fatty acids Pub Date : 2003-05-01 DOI:10.1016/S0952-3278(03)00021-8

I. Sato , A. Suzuki , A. Kakita , Y. Ono , Y. Miura , M. Itoh , Y. Oiso

{"title":"前列腺素F(2α)对na依赖性磷酸盐在成骨细胞样细胞中的转运的刺激作用。","authors":"I. Sato , A. Suzuki , A. Kakita , Y. Ono , Y. Miura , M. Itoh , Y. Oiso","doi":"10.1016/S0952-3278(03)00021-8","DOIUrl":null,"url":null,"abstract":"<div><div>Prostaglandin F2α (PGF2α) has been reported to activate protein kinase C (PKC) through both phospholipase (PL) C and D, resulting in the proliferation of osteoblast-like cells. In addition, it has also been reported that Erk mitogen-activated protein kinase is also involved in the mechanism of PGF2α-induced proliferation of these cells. Recently, we have reported that several growth factors stimulate Na-dependent phosphate transport (Pi transport) activity of osteoblast-like cells, which has been recognized to play an important role in their mineralization. In the present study, we investigated the effect of PGF2α on Pi transport in MC3T3-E1 osteoblast-like cells. PGF2α stimulated Na-dependent Pi transport dose dependently in the range between 1nM and 10μM in MC3T3-E1 cells. The effect was time dependent up to 24h. Kinetic analysis revealed that PGF2α induces newly synthesized Pi transporter. Pretreatment with actinomycin D and cycloheximide suppressed PGF2α-induced enhancement of Pi transport. Combined effect of PMA and PGF2α was not additive in Pi transport. Calphostin C, a PKC inhibitor, dose-dependently suppressed Pi transport induced by PGF2α. On the contrary, U0126, which inhibits an upstream kinase of Erk (MEK), did not affect PGF2α-induced enhancement of Pi transport.</div><div>In conclusion, PGF2α stimulates Pi transport through activation of PKC in osteoblast-like cells.</div></div>","PeriodicalId":94179,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"68 5","pages":"Pages 311-315"},"PeriodicalIF":3.0000,"publicationDate":"2003-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Stimulatory effect of prostaglandin F2α on Na-dependent phosphate transport in osteoblast-like cells\",\"authors\":\"I. Sato , A. Suzuki , A. Kakita , Y. Ono , Y. Miura , M. Itoh , Y. Oiso\",\"doi\":\"10.1016/S0952-3278(03)00021-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Prostaglandin F2α (PGF2α) has been reported to activate protein kinase C (PKC) through both phospholipase (PL) C and D, resulting in the proliferation of osteoblast-like cells. In addition, it has also been reported that Erk mitogen-activated protein kinase is also involved in the mechanism of PGF2α-induced proliferation of these cells. Recently, we have reported that several growth factors stimulate Na-dependent phosphate transport (Pi transport) activity of osteoblast-like cells, which has been recognized to play an important role in their mineralization. In the present study, we investigated the effect of PGF2α on Pi transport in MC3T3-E1 osteoblast-like cells. PGF2α stimulated Na-dependent Pi transport dose dependently in the range between 1nM and 10μM in MC3T3-E1 cells. The effect was time dependent up to 24h. Kinetic analysis revealed that PGF2α induces newly synthesized Pi transporter. Pretreatment with actinomycin D and cycloheximide suppressed PGF2α-induced enhancement of Pi transport. Combined effect of PMA and PGF2α was not additive in Pi transport. Calphostin C, a PKC inhibitor, dose-dependently suppressed Pi transport induced by PGF2α. On the contrary, U0126, which inhibits an upstream kinase of Erk (MEK), did not affect PGF2α-induced enhancement of Pi transport.</div><div>In conclusion, PGF2α stimulates Pi transport through activation of PKC in osteoblast-like cells.</div></div>\",\"PeriodicalId\":94179,\"journal\":{\"name\":\"Prostaglandins, leukotrienes, and essential fatty acids\",\"volume\":\"68 5\",\"pages\":\"Pages 311-315\"},\"PeriodicalIF\":3.0000,\"publicationDate\":\"2003-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Prostaglandins, leukotrienes, and essential fatty acids\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0952327803000218\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Prostaglandins, leukotrienes, and essential fatty acids","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0952327803000218","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 0

摘要

据报道，前列腺素F(2alpha) (PGF(2alpha))通过磷脂酶(PL) C和D激活蛋白激酶C (PKC)，导致成骨细胞样细胞增殖。此外，也有报道称Erk丝裂原活化蛋白激酶也参与了PGF(2alpha)诱导这些细胞增殖的机制。最近，我们报道了几种生长因子刺激Na-dependent phosphate transport (Pi transport)活性，这在成骨细胞样细胞的矿化中起重要作用。在本研究中，我们研究了PGF(2alpha)对MC3T3-E1成骨样细胞中Pi转运的影响。在MC3T3-E1细胞中，PGF(2alpha)在1nM ~ 10 micro - M范围内以剂量依赖性刺激na依赖的Pi转运。效果与时间有关，最长可达24小时。动力学分析表明PGF(2alpha)诱导新合成的Pi转运体。放线菌素D和环己亚胺预处理可抑制PGF(2alpha)诱导的Pi转运增强。PMA和PGF(2alpha)的联合作用在Pi转运中不加和。Calphostin C, PKC抑制剂，剂量依赖性地抑制PGF(2alpha)诱导的Pi转运。相反，抑制Erk上游激酶(MEK)的U0126不影响PGF(2alpha)诱导的Pi转运增强。综上所述，PGF(2alpha)通过激活成骨细胞样细胞中的PKC刺激Pi转运。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

Stimulatory effect of prostaglandin F2α on Na-dependent phosphate transport in osteoblast-like cells

Prostaglandin F_2α (PGF_2α) has been reported to activate protein kinase C (PKC) through both phospholipase (PL) C and D, resulting in the proliferation of osteoblast-like cells. In addition, it has also been reported that Erk mitogen-activated protein kinase is also involved in the mechanism of PGF_2α-induced proliferation of these cells. Recently, we have reported that several growth factors stimulate Na-dependent phosphate transport (Pi transport) activity of osteoblast-like cells, which has been recognized to play an important role in their mineralization. In the present study, we investigated the effect of PGF_2α on Pi transport in MC3T3-E1 osteoblast-like cells. PGF_2α stimulated Na-dependent Pi transport dose dependently in the range between 1 nM and 10 μM in MC3T3-E1 cells. The effect was time dependent up to 24 h. Kinetic analysis revealed that PGF_2α induces newly synthesized Pi transporter. Pretreatment with actinomycin D and cycloheximide suppressed PGF_2α-induced enhancement of Pi transport. Combined effect of PMA and PGF_2α was not additive in Pi transport. Calphostin C, a PKC inhibitor, dose-dependently suppressed Pi transport induced by PGF_2α. On the contrary, U0126, which inhibits an upstream kinase of Erk (MEK), did not affect PGF_2α-induced enhancement of Pi transport.

In conclusion, PGF_2α stimulates Pi transport through activation of PKC in osteoblast-like cells.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

来源期刊