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首页> 外文期刊>Materials science & engineering >High-phosphorus environment promotes calcification of A7R5 cells induced by hydroxyapatite nanoparticles
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High-phosphorus environment promotes calcification of A7R5 cells induced by hydroxyapatite nanoparticles

机译：高磷环境促进羟基磷灰石纳米颗粒诱导的A7R5细胞钙化

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摘要

This study simulated the high-phosphorus (Pi) environment in patients with chronic kidney disease. Nano-hydroxyapatite (HAP) crystals were used to damage rat aortic smooth muscle cells (A7R5) pre-damaged with different concentrations of Pi solution to compare the differences in HAP-induced calcification in A7R5 cells before and after injury by high-Pi condition. After the A7R5 cells were damaged by high-Pi environment, the following were observed. HAP resulted in declined cell viability and lysosomal integrity, release of lactate dehydrogenase, and increased reactive oxygen species production. The ability of high-Pi damaged cells to internalize HAP crystals declined; crystal adhesion and calcium deposition on the cell surface and alkaline phosphatase activities increased. Osteopontin expression and level of Runt-related transcription factor 2 were increased, and HAP-induced osteogenic transformation was enhanced. High-Pi condition promoted the adhesion of A7R5 cells to nano-HAP crystals and inhibited HAP endocytosis, increasing the risk of calcification.
机译：这项研究模拟了慢性肾脏病患者的高磷（Pi）环境。纳米羟基磷灰石（HAP）晶体用于损伤预先用不同浓度的Pi溶液损伤的大鼠主动脉平滑肌细胞（A7R5），以比较高Pi条件损伤前后HAP诱导的A7R5细胞钙化的差异。在高Pi环境损坏A7R5细胞后，观察到以下情况。 HAP导致细胞活力和溶酶体完整性下降，乳酸脱氢酶释放以及活性氧产生增加。高Pi损伤的细胞将HAP晶体内在化的能力下降；晶体粘附和细胞表面钙沉积和碱性磷酸酶活性增加。骨桥蛋白的表达和Runt相关转录因子2的水平增加，并且HAP诱导的成骨转化增强。高Pi条件促进A7R5细胞与纳米HAP晶体的粘附并抑制HAP内吞作用，增加钙化的风险。

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