Cardiac microvascular damage, which is often caused by anoxia and hypoglycemia, is associated with the development of cardiac injury. DJ-1 encodes a peptidase C56 protein family related protein, is has been linked to oxidative stress in various cells such as neurons, COPD epithelial cells, and macrophages. However, the effect of DJ-1 towards oxidative stress caused by anoxia and hypoglycemia of cardiac microvascular endothelial cells (CMEC) remains unclear. In this study, we investigated the role and underlying molecular mechanism of DJ-1 in CMEC with anoxia/hypoglycemic (A/H) injury. We found that the mRNA and the protein expression of DJ-1 in CMEC with A/H injury were significantly downregulated. DJ-1 overexpression by pcDNA.3.1-DJ-1 transfection elevated cell viability while it inhibited LDH leakage, cell apoptosis, caspase-3 activity, ROS level, and MDA contents, while knockdown of DJ-1 has the opposite results. In addition, tube formation was increased in DJ-1 overexpression, while it was decreased in DJ-1 knockdown CMEC with A/H injury. In addition, our results indicated that DJ-1 can regulate glutathione (GSH) levels by modulating AKT activity in CMEC with A/H injury. The downregulation of AKT and GSH may remove the protective role of DJ-1 against A/H injury in CMEC. Taken together, this study showed that DJ-1 upregulation protected CMEC against A/H injury via the AKT/GSH signaling pathway.

中文翻译：

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DJ-1可通过AKT和GSH减轻心脏微血管的缺氧和低血糖损伤。

经常由缺氧和低血糖引起的心脏微血管损伤与心脏损伤的发展有关。DJ-1编码肽酶C56蛋白家族相关蛋白，已与各种细胞（如神经元，COPD上皮细胞和巨噬细胞）的氧化应激相关。但是，DJ-1对由心脏微血管内皮细胞（CMEC）的缺氧和低血糖引起的氧化应激的作用尚不清楚。在这项研究中，我们调查了DJ-1在缺氧/低血糖（A / H）损伤的CMEC中的作用及其潜在的分子机制。我们发现A / H损伤的CMEC中DJ-1的mRNA和蛋白表达明显下调。pcDNA.3.1-DJ-1转染DJ-1过表达可提高细胞活力，同时抑制LDH泄漏，细胞凋亡，caspase-3活性，ROS水平和MDA含量，而击倒DJ-1的结果相反。此外，在DJ-1过表达中，随着A / H损伤，管形成增加，而在DJ-1敲低CMEC中，管形成减少。此外，我们的结果表明，DJ-1可以通过调节A / H损伤的CMEC中的AKT活性来调节谷胱甘肽（GSH）水平。AKT和GSH的下调可能会消除DJ-1对CMEC中A / H损伤的保护作用。两者合计，这项研究表明DJ-1上调通过AKT / GSH信号通路保护CMEC免受A / H损伤。我们的结果表明，DJ-1可以通过调节A / H损伤的CMEC中的AKT活性来调节谷胱甘肽（GSH）的水平。AKT和GSH的下调可能会消除DJ-1对CMEC中A / H损伤的保护作用。两者合计，这项研究表明DJ-1上调通过AKT / GSH信号通路保护CMEC免受A / H损伤。我们的结果表明，DJ-1可以通过调节A / H损伤的CMEC中的AKT活性来调节谷胱甘肽（GSH）的水平。AKT和GSH的下调可能会消除DJ-1对CMEC中A / H损伤的保护作用。两者合计，这项研究表明DJ-1上调通过AKT / GSH信号通路保护CMEC免受A / H损伤。