Hypoxic preconditioning promotes the immunosuppressive effects of mesenchymal stem cells in mice with colitis.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Mesenchymal stem cells are promising candidates for stem cell therapy in many diseases, especially in immune-associated diseases. Inflammatory bowel disease is a chronic autoimmune disease that can lead to colorectal cancer if it is not controlled. Mesenchymal stem cells are always under a hypoxic environment in vivo, whether in bone marrow or adipose tissue, whereas researchers always culture MSCs (mesenchymal stem cells) under normoxic conditions (21%). In this study, we aimed to investigate whether hypoxia (1%) affects the therapeutic effect of MSCs. We hypothesize that hypoxia may benefit the treatment efficacy of MSCs. We used DSS to induce IBD (inflammatory bowel disease) in mice and then injected MSCs that had been preconditioned under normoxic conditions (21%) and hypoxic conditions (1%). We found that compared with normoxic-preconditioned MSCs (n-MSCs), hypoxic-preconditioned MSCs (h-MSCs) could alleviate colon inflammation to a large extent, as determined by inflammatory cytokines and CD3 + T cell activation. Mechanistic studies showed that hypoxia could promote iNOS expression in MSCs. Therefore, our data suggest that hypoxia may be more appropriate than normoxia for facilitating MSCs exertion of therapeutic functions.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.