Human umbilical cord-derived mesenchymal stem cells alleviate oxidative stress-induced islet impairment via the Nrf2/HO-1 axis.
Peng LiuBaige CaoYang ZhouHuina ZhangCongrong WangPublished in: Journal of molecular cell biology (2023)
Hyperglycaemia-induced oxidative stress may disrupt insulin secretion and β-cell survival in diabetes mellitus by overproducing reactive oxygen species. Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) exhibit anti-oxidant properties. However, the mechanisms by which hUC-MSCs protect β-cells from high glucose-induced oxidative stress remain underexplored. In this study, we showed that intravenous injection of hUC-MSCs engrafted into the injured pancreas and promoted pancreatic β-cell function in a mouse model of type 1 diabetes mellitus. In vitro study revealed that hUC-MSCs attenuated high glucose-induced oxidative stress and prevented β-cell impairment via the Nrf2/HO-1 signaling pathway. Nrf2 knockdown partially blocked the anti-oxidative effect of hUC-MSCs, resulting in β-cell decompensation in a high glucose environment. Overall, these findings provide novel insights into how hUC-MSCs protect β-cells from high glucose-induced oxidative stress.
Keyphrases
- high glucose
- umbilical cord
- endothelial cells
- mesenchymal stem cells
- cell therapy
- hydrogen peroxide
- oxidative stress
- single cell
- signaling pathway
- bone marrow
- reactive oxygen species
- mouse model
- pi k akt
- epithelial mesenchymal transition
- type diabetes
- metabolic syndrome
- weight loss
- cell proliferation
- pluripotent stem cells
- induced pluripotent stem cells
- nitric oxide