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首页> 外文期刊>Journal of cellular physiology. >Type 2 diabetes-induced hyposalivation of the submandibular gland through PINKl/Parkin-mediated mitophagy
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Type 2 diabetes-induced hyposalivation of the submandibular gland through PINKl/Parkin-mediated mitophagy

机译：2型diabetes-induced hyposalivation的通过PINKl / Parkin-mediated颌下腺

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Diabetes is often accompanied by dysfunction of salivary glands. However, the molecular mechanism remains unclear. The mechanisms that underlie diabetic hyposalivation were studied by db/db mice and SMG-C6 cells. We found morphological changes and decreased stimulated salivary flow rates of the submandibular gland (SMG) in diabetic mice. We observed structural changes and dysfunction of mitochondria. More mitophagosomes and higher expression of autophagy-related proteins were detected. Increased levels of proteins PINK1 and Parkin indicate that PINKl/Parkin-mediated mitophagy was activated in diabetic SMG. Consistently, high glucose (HG) induced mitochondrial dysfunction and PINKl/Parkin-mediated mitophagy in cultivated SMG-C6 cells. HG also increased reactive oxygen species (ROS) and lessened activation of antioxidants in SMG-C6 cells. In addition, HG lowered ERK1/2 phosphorylation and HG-induced mitophagy was decreased after ERK1/2 was activated by LM22B-10. Altogether, these data suggest that ROS played a crucial role in diabetes-induced mitochondrial dysfunction and PINKl/Parkin-mediated mitophagy and ERK1/2 was required in HG-induced mitophagy in SMG.
机译：糖尿病常伴有功能障碍唾液腺。仍不清楚。糖尿病hyposalivation研究了db / db老鼠和SMG-C6细胞。变化和减少刺激唾液流利率的颌下腺(SMG)糖尿病小鼠。线粒体功能障碍。和更高的autophagy-related的表情蛋白质检测。蛋白质PINK1和帕金表明PINKl / Parkin-mediated mitophagy被激活糖尿病SMG。诱导线粒体功能障碍和PINKl / Parkin-mediated mitophagy栽培SMG-C6细胞。物种(ROS)和减少激活抗氧化剂SMG-C6细胞。降低ERK1/2磷酸化和HG-inducedmitophagy ERK1/2后下降由LM22B-10激活。表明,ROS起到了至关重要的作用diabetes-induced线粒体功能障碍和PINKl / Parkin-mediated mitophagy和ERK1/2需要HG-induced mitophagy SMG。

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