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首页> 外文期刊>American Journal of Physiology >Knockdown of ERp57 increases BiP/GRP78 induction and protects against hyperoxia and tunicamycin-induced apoptosis.
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Knockdown of ERp57 increases BiP/GRP78 induction and protects against hyperoxia and tunicamycin-induced apoptosis.

机译：敲除ERp57可以增加BiP / GRP78的诱导，并防止高氧和衣霉素诱导的细胞凋亡。

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摘要

Supplemental oxygen therapy (hyperoxia) in preterm babies with respiratory stress is associated with lung injury and the development of bronchopulmonary dysplasia. Endoplasmic reticulum (ER) homeostasis plays critical roles in maintaining cellular functions such as protein synthesis, folding, and secretion. Interruption of ER homeostasis causes ER stress and triggers the unfolded protein response, which can lead to apoptosis in persistently stressed cells. ERp57 is an ER protein and is associated with calreticulin and calnexin in protein glycosylation. In this study, we found hyperoxia downregulated ERp57 in neonatal rat lungs and cultured human endothelial cells. Transient transfection of ERp57 small interfering RNA significantly knocked down ERp57 expression and reduced hyperoxia- or tunicamycin-induced apoptosis in human endothelial cells. Apoptosis was decreased from 26.8 to 9.9% in hyperoxia-exposed cells and from 37.8 to 5.0% in tunicamycin-treated cells. The activation of caspase-3 induced by hyperoxia or tunicamycin was diminished and immunoglobulin heavy chain-binding protein/glucose-regulated protein 78-kDa (BiP/GRP78) induction was increased in ERp57 knockdown cells. Overexpression of ERp57 exacerbated hyperoxia- or tunicamycin-induced apoptosis in human endothelial cells. Apoptosis was increased from 10.1 to 14.3% in hyperoxia-exposed cells and from 14.0 to 21.2% in tunicamycin-treated cells. Overexpression of ERp57 also augmented tunicamycin-induced caspase-3 activation and reduced BiP/GRP78 induction. Our results demonstrate that ERp57 can regulate apoptosis in human endothelial cells. It appears that knockdown of ERp57 confers cellular protection against hyperoxia- or tunicamycin-induced apoptosis by inhibition of caspase-3 activation and stimulation of BiP/GRP78 induction.
机译：患有呼吸道压力的早产婴儿的补充氧气治疗（高氧血症）与肺损伤和支气管肺发育不良有关。内质网（ER）稳态在维持细胞功能（如蛋白质合成，折叠和分泌）中起关键作用。内质网稳态的中断会引起内质网应激并触发未折叠的蛋白质反应，从而导致持续应激的细胞凋亡。 ERp57是一种ER蛋白，在蛋白糖基化过程中与钙网蛋白和钙联接蛋白相关。在这项研究中，我们发现高氧在新生大鼠肺和培养的人内皮细胞中下调了ERp57。瞬时转染ERp57小干扰RNA会显着降低ERp57的表达，并减少高氧或衣霉素诱导的人内皮细胞凋亡。高氧暴露细胞的凋亡从26.8％降低到9.9％，衣霉素处理细胞的凋亡从37.8％降低到5.0％。高氧或衣霉素诱导的caspase-3的激活减少，ERp57敲低细胞中免疫球蛋白重链结合蛋白/葡萄糖调节蛋白78-kDa（BiP / GRP78）的诱导增加。 ERp57的过表达加剧了高氧或衣霉素诱导的人内皮细胞凋亡。高氧暴露细胞的凋亡从10.1％增加到14.3％，衣霉素处理细胞的凋亡从14.0％增加到21.2％。 ERp57的过表达还增强了衣霉素诱导的caspase-3激活并降低了BiP / GRP78诱导。我们的结果表明，ERp57可以调节人内皮细胞的凋亡。看来，敲低ERp57可以通过抑制caspase-3活化和刺激BiP / GRP78诱导而赋予细胞针对高氧或衣霉素诱导的细胞凋亡的保护作用。

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