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Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
Published on: May 21, 2012
The m6A reader HNRNPC is a key regulator in DSS-induced colitis by modulating macrophage phenotype
Xiaohui Fang1,2, Yu Zhang1,2, Ziliang Ke1,2
1Department of Gastroenterology, Peking University Peoples Hospital, No.11, Xizhimen South Street, Xicheng District, Beijing 100044, China.
Abstract:
m6A regulators were demonstrated to modulate the functions of intestinal epithelial and immune cells in the ulcerative colitis. This study aimed to elucidate whether and how the m6A reader heterogeneous nuclear ribonucleoprotein C (HNRNPC) regulates macrophage function in the colitis. We observed elevated HNRNPC in the inflammatory Raw264.7 cells and macrophages in the dextran sodium sulfate (DSS)-induced colitis. Knocking down HNRNPC can mitigate LPS-induced activation of macrophages in vitro. Furthermore, adoptive transfer of macrophages with HNRNPC knockdown significantly alleviated colitis compared to those transfected with negative control siRNA. Additionally, RNA sequencing illuminated that HNRNPC regulated functions of macrophages by inhibiting alternative mRNA slicing, involving adjusting acute inflammatory response, and promoting cell chemotaxis and migration. Besides, HNRNPC can govern the stability of Itgb7, and Itgb7 might be an effective target for HNRNPC in macrophages. Our findings highlight the crucial role and therapeutic potential of HNRNPC inhibition in macrophages in alleviating colitis.
Insights
Heterogeneous nuclear ribonucleoprotein C (HNRNPC) regulates macrophage function in ulcerative colitis. Inhibiting HNRNPC in macrophages alleviates colitis by modulating inflammation and cell migration, showing therapeutic potential.
Area of Science:
- Immunology
- Molecular Biology
- Gastroenterology
Background:
- m6A regulators influence intestinal epithelial and immune cells in ulcerative colitis.
- The role of the m6A reader heterogeneous nuclear ribonucleoprotein C (HNRNPC) in macrophage function during colitis is unclear.
Purpose of the Study:
- To investigate how HNRNPC regulates macrophage function in the context of colitis.
- To explore the therapeutic potential of targeting HNRNPC in macrophages for ulcerative colitis treatment.
Main Methods:
- Utilized dextran sodium sulfate (DSS)-induced colitis model in mice.
- Performed in vitro studies involving LPS-induced macrophage activation.
- Conducted RNA sequencing to identify HNRNPC-regulated pathways.
- Assessed the effect of adoptive transfer of HNRNPC-knockdown macrophages in colitis models.
Main Results:
- HNRNPC expression was elevated in inflammatory cells and macrophages during DSS-induced colitis.
- HNRNPC knockdown reduced LPS-induced macrophage activation in vitro.
- Adoptive transfer of HNRNPC-knockdown macrophages significantly ameliorated colitis.
- RNA sequencing revealed HNRNPC inhibits alternative mRNA splicing, modulates inflammatory responses, and promotes cell chemotaxis and migration.
- HNRNPC influences the stability of Itgb7, a potential therapeutic target.
Conclusions:
- HNRNPC plays a critical role in regulating macrophage function during colitis.
- Inhibiting HNRNPC in macrophages presents a promising therapeutic strategy for ulcerative colitis.
