• Medientyp: E-Book
  • Titel: Long-Term Environmental Levels of Microcystin-Lr Exposure Induces Colorectal Chronic Inflammation, Fibrosis and Barrier Disruption Via Csf1r/Rap1b Signaling Pathway
  • Beteiligte: Yang, Yue [VerfasserIn]; Wang, Hui [VerfasserIn]; Liu, Wenya [VerfasserIn]; Cai, Danping [VerfasserIn]; Chu, Hanyu [VerfasserIn]; Deng, Shuxiang [VerfasserIn]; Liu, Ying [VerfasserIn]; Tang, Yan [VerfasserIn]; Feng, Xiangling [VerfasserIn]; Chen, Jihua [VerfasserIn]; Wang, Chengkun [VerfasserIn]; Pu, Yuepu [VerfasserIn]; Ding, Zhen [VerfasserIn]; Li, Guoqing [VerfasserIn]; Cao, Yi [VerfasserIn]; Long, Dingxin [VerfasserIn]; Wang, Xiaoyan [VerfasserIn]; Yang, Fei [VerfasserIn]
  • Erschienen: [S.l.]: SSRN, [2022]
  • Umfang: 1 Online-Ressource (28 p)
  • Sprache: Englisch
  • DOI: 10.2139/ssrn.4023886
  • Identifikator:
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: Microcystin-LR (MC-LR) is the most toxic cyanotoxins threating ecosystems and the public health. This study aims to explore the long-term effects and potential toxicity mechanisms of MC-LR exposure at environmental levels on colorectal injury. We performed histopathological, biochemical indicator and multi-omics analyses in mice with low-dose MC-LR exposure for 12 months. Long-term environmental levels of MC-LR exposure caused epithelial barrier disruption, inflammatory cell infiltration and an increase of collagen fibers in mouse colorectum. Integrated proteotranscriptomics revealed differential expression of genes/proteins, including CSF1R, which were mainly involved in oxidative stress-induced premature senescence and inflammatory response. MC-LR induced chronic inflammation and fibrosis through oxidative stress and CSF1R/Rap1b signaling pathway were confirmed in cell models. We found for the first time that long-term environmental levels of MC-LR exposure caused colorectal chronic inflammation, fibrosis and barrier disruption via a novel CSF1R/Rap1b signaling pathway. Moreover, MC-LR changed the gut microbiota and microbial-related metabolites in a vicious circle aggravating colorectal injury. These findings provide novel insights into the effects and toxic mechanisms of MC-LR and suggest strategies for the prevention and treatment of MC-caused intestinal diseases
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