Promotion on Nucleation and Aggregation of Calcium Oxalate Crystals by Injury of HKC Cell
Promotion on Nucleation and Aggregation of Calcium Oxalate Crystals by Injury of HKC Cell
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HKC细胞损伤促进草酸钙晶体成核和聚集
DOI：
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发表时间：
2011
期刊：
影响因子：
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通讯作者：
Ouyang Jian-Ming
中科院分区：
文献类型：
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作者：
Yao Xiu-Qiong;Deng Sui-Ping;Ouyang Jian-Ming
H2O2损伤人肾小管上皮细胞（HKC），细胞损伤导致HKC存活率下降，骨桥蛋白（OPN）表达增加，随着损伤时间的延长，细胞存活率持续下降，OPN表达也持续增加，与对照组相比，损伤细胞诱导的晶体数量明显增加，晶体聚集水平也增加，但对草酸钙晶体生长的影响不明显，对照细胞主要诱导二水草酸钙（COD）晶体的形成，受损细胞同时诱导形成更大量的草酸钙一水合物（COM）结果表明，在一定条件下，草酸钙晶体的成核、聚集和COM晶体的形成均得到了促进。肾小管上皮细胞损伤可能增加肾结石形成的风险。
Human renal tubular epithelial cells(HKC) were injured by H2O2.Cell damage caused the decreased viability of HKC,and the increased expression of osteopontin(OPN).With the injury time increased,cell viability continued to decline,and OPN expression also increased continuously.Compared to control cells,the number of crystals induced by the damaged cells increased significantly,and the aggregation level of the crystal also increased,but the effect on growth of calcium oxalate crystals was not significant.The control cells mainly induced formation of calcium oxalate dihydrate(COD) crystals.However,the damaged cells simultaneously induced formation of a greater amount of calcium oxalate monohydrate(COM).This indicated that both the nucleation and aggregation of calcium oxalate crystals and the formation of COM crystals were promoted.The results suggest that damage of renal tubular epithelial cells might increase the risk of kidney stone formation.