胶质细胞源性神经生长因子
神经营养因子
结肠炎
下调和上调
促炎细胞因子
巨噬细胞
炎症
小胶质细胞
PI3K/AKT/mTOR通路
癌症研究
免疫学
巨噬细胞极化
蛋白激酶B
化学
细胞生物学
药理学
信号转导
医学
生物
内科学
生物化学
受体
体外
基因
作者
Jian Zeng,Huan Yu,Hua‐Tian Gan
标识
DOI:10.1016/j.intimp.2021.108143
摘要
Glial cell line-derived neurotrophic factor (GDNF) has been reported to protect mice from intestinal inflammation, but its anti-inflammatory mechanisms are poorly understood. Here we found that there was a downregulation in intestinal expression of GDNF accompanied by an increase of M1 macrophages in dextran sulfate sodium (DSS)-induced colitis in mice. GDNF treatment could facilitate the macrophages polarization towards the M2-like phenotype in DSS-treated mice and LPS-stimulated RAW264.7 cells, and reduce pro-inflammatory cytokines and increase anti-inflammatory cytokines. Mechanistically, the activation of PI3K/AKT pathway might contribute to the regulation of GDNF on macrophage phenotypes and inflammatory response. Moreover, the administration of GDNF significantly ameliorated colitis in DSS-treated mice, but this benefit of GDNF was diminished by macrophage depletion. Therefore, we propose a new mechanism whereby GDNF suppresses DSS-induced colitis in mice via a macrophage-mediated pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI