Wieland Fredrik C, Sthijns Mireille M J P E, Geuens Thomas, van Blitterswijk Clemens A, LaPointe Vanessa L S
MERLN Institute for Technology-Inspired Regenerative Medicine, Maastricht University, Maastricht, Netherlands.
Centre for Healthy Eating and Food Innovation, Maastricht University, Maastricht, Netherlands.
Front Bioeng Biotechnol. 2021 Sep 9;9:729057. doi: 10.3389/fbioe.2021.729057. eCollection 2021.
Pancreatic beta cells have inadequate levels of antioxidant enzymes, and the damage induced by oxidative stress poses a challenge for their use in a therapy for patients with type 1 diabetes. It is known that the interaction of the pancreatic endocrine cells with support cells can improve their survival and lead to less vulnerability to oxidative stress. Here we investigated alpha (alpha TC-1), beta (INS1E) and endothelial (HUVEC) cells assembled into aggregates known as pseudoislets as a model of the pancreatic islets of Langerhans. We hypothesised that the coculture of alpha, beta and endothelial cells would be protective against oxidative stress. First, we showed that adding endothelial cells decreased the percentage of oxidative stress-positive cells. We then asked if the number of endothelial cells or the size (number of cells) of the pseudoislet could increase the protection against oxidative stress. However, no additional benefit was observed by those changes. On the other hand, we identified a potential supportive effect of the alpha cells in reducing oxidative stress in beta and endothelial cells. We were able to link this to the incretin glucagon-like peptide-1 (GLP-1) by showing that the absence of alpha cells in the pseudoislet caused increased oxidative stress, but the addition of GLP-1 could restore this. Together, these results provide important insights into the roles of alpha and endothelial cells in protecting against oxidative stress.
胰腺β细胞的抗氧化酶水平不足,氧化应激诱导的损伤对其用于1型糖尿病患者的治疗构成了挑战。已知胰腺内分泌细胞与支持细胞的相互作用可提高其存活率,并降低对氧化应激的易感性。在这里,我们研究了组装成称为假胰岛的聚集体的α(αTC-1)、β(INS1E)和内皮(HUVEC)细胞,作为朗格汉斯胰岛的模型。我们假设α、β和内皮细胞的共培养对氧化应激具有保护作用。首先,我们发现添加内皮细胞可降低氧化应激阳性细胞的百分比。然后我们询问内皮细胞的数量或假胰岛的大小(细胞数量)是否可以增强对氧化应激的保护作用。然而,这些变化并未观察到额外的益处。另一方面,我们发现α细胞在降低β和内皮细胞氧化应激方面具有潜在的支持作用。我们通过证明假胰岛中缺乏α细胞会导致氧化应激增加,但添加胰高血糖素样肽-1(GLP-1)可以恢复这一点,将其与肠促胰岛素GLP-1联系起来。总之,这些结果为α和内皮细胞在抵抗氧化应激中的作用提供了重要见解。