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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Role of endoplasmic reticulum stress pathway in hydrostatic pressure-induced apoptosis in rat mandibular condylar chondrocytes
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Role of endoplasmic reticulum stress pathway in hydrostatic pressure-induced apoptosis in rat mandibular condylar chondrocytes

机译：内质网应激途径在大鼠颌骨髁突软骨细胞静压压力诱导细胞凋亡中的作用

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摘要

Excessive mechanical loads induce chondrocyte apoptosis and irreversible cartilage degeneration, but the underlying molecular mechanism is poorly understood. The aim of this study was to investigate the possible role of endoplasmic reticulum (ER) stress pathway in hydrostatic pressure (HP)-induced apoptosis in rat mandibular condylar chondrocytes. Chondrocytes were isolated from rat mandibular condylar cartilage and subjected to HP. Cell viability and apoptosis were assessed by Cell Counting Kit-8 and flow cytometry assay. Expression of ER stress-associated molecules was detected by quantitative real-time PCR and western blot analysis. In addition, expression of apoptosis-related proteins (bax, bcl-2, and cleaved-caspase-3) was assessed by western blot. To explore ER stress function, chondrocytes were pretreated with salubrinal before exposure to HP. Expression of type II collagen, aggrecan, MMP13, and ADAMTS-5 was evaluated by real-time PCR. The results indicated that HP reduced cell viability in a magnitude-and time-dependent manner. HP-induced activation of ER stress pathway by increasing expression of GRP78, CHOP, caspase-12, PERK, and peIF2 alpha in chondrocytes. Moreover, the expression of bax and cleaved-caspase-3 was increased, while the expression of bcl-2 was decreased in response to HP as the stress time prolonged. In addition, salubrinal suppressed HP-induced apoptosis, upregulated type II collagen and aggrecan mRNA expression, and downregulated MMP-13 and ADAMTS-5 mRNA expression in response to HP. These results demonstrate that HP induces apoptosis in mandibular condylar chondrocytes through ER stress-mediated apoptotic pathway. Suppression of ER stress by salubrinal prevents chondrocytes from undergoing apoptosis and matrix degradation induced by HP.
机译：机械载荷过多诱导软骨细胞凋亡和不可逆的软骨变性，但潜在的分子机制理解得很差。本研究的目的是探讨内质网（ER）应激途径在静压压力（HP）中的可能作用 - 诱导大鼠颌骨髁骨软骨细胞的细胞凋亡。从大鼠颌骨髁软骨中分离出软骨细胞并进行HP。通过细胞计数试剂盒-8和流式细胞术测定评估细胞活力和细胞凋亡。通过定量实时PCR和Western印迹分析检测ER应激相关分子的表达。此外，通过Western印迹评估凋亡相关蛋白质（BAX，BCL-2和Celeave-Caspase-3）的表达。为了探索ER应激功能，在暴露于HP之前用盐酸盐预处理软骨细胞。通过实时PCR评估II型胶原蛋白，蛋白，MMP13和Adamts-5的表达。结果表明，HP以大小和时间依赖的方式降低了细胞活力。通过增加GRP78，Chop，Caspase-12，Perk和PeiF2α的表达，HP诱导激活ER应激途径。此外，增加了Bax和切割的 - caspase-3的表达，而Bcl-2的表达响应于HP而随着应力时间延长而降低。此外，Salubrinal抑制了HP诱导的凋亡，上调II型胶原和聚合物mRNA表达，并响应于HP，下调的MMP-13和Adamts-5 mRNA表达。这些结果表明，HP通过ER应激介导的凋亡途径诱导颌骨髁突骨细胞细胞凋亡。 Salubrinal抑制ER应力可防止软骨细胞经历HP诱导的细胞凋亡和基质降解。

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