Prohibitin is an evolutionarily conserved and ubiquitously expressed protein in eukaryocyte. It mediate many important roles in cell survival, apoptosis, autophagy and senescence. In the present study, we aimed to explore the role of prohibitin in cigarette smoke extract (CSE)-induced apoptosis of human pulmonary microvascular endothelial cells (HPMECs). For this purpose, HPMECs were trasfected with prohibitin and challenged with CSE. Our results showed that CSE exposure inhibited prohibitin expression in a dose-dependent manner in HPMECs. Overexpression of prohibitin could protect cell from CSE-induced injury by inhibiting CSE-induced cell apoptosis, inhibiting reactive oxygen species (ROS) production, increase mitochondrial membrane potential, increase the content of mitochondrial transcription factor A (mtTFA), IKKα/β phosphorylation and IκB-α degradation. CSE decreases prohibitin expression in endothelial cells and restoration of prohibitin expression in these cells can protect against the deleterious effects of CSE on mitochondrial and cells. We identified prohibitin is a novel regulator of endothelial cell apoptosis and survival in the context of cigarette smoke exposure.

中文翻译：

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抑制素可防止香烟烟雾提取物诱导的人肺微血管内皮细胞凋亡

抑制素是真核细胞中进化上保守的和普遍表达的蛋白。它在细胞存活，凋亡，自噬和衰老中起着许多重要的作用。在本研究中，我们旨在探讨禁止素在香烟烟雾提取物（CSE）诱导的人肺微血管内皮细胞（HPMEC）凋亡中的作用。为此，将HPMECs用禁止素转染并用CSE攻击。我们的结果表明，CSE暴露以剂量依赖的方式抑制HPMEC中的禁止素表达。禁止素的过度表达可通过抑制CSE诱导的细胞凋亡，抑制活性氧（ROS）产生，增加线粒体膜电位，增加线粒体转录因子A（mtTFA）的含量来保护细胞免受CSE诱导的损伤，IKKα/β磷酸化和IκB-α降解。CSE降低了内皮细胞中禁止素的表达，而这些细胞中禁止素的表达恢复可以防止CSE对线粒体和细胞的有害作用。我们确定禁止素是香烟烟雾暴露背景下内皮细胞凋亡和存活的新型调节剂。