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• W2911247714 abstract "Background & AimsLevels of microRNA 31 (MIR31) are increased in intestinal tissues from patients with inflammatory bowel diseases and colitis-associated neoplasias. We investigated the effects of this microRNA on intestinal inflammation by studying mice with colitis.MethodsWe obtained colon biopsy samples from 82 patients with ulcerative colitis (UC), 79 patients with Crohn’s disease (CD), and 34 healthy individuals (controls) at Shanghai Tenth People’s Hospital. MIR31- knockout mice and mice with conditional disruption of Mir31 specifically in the intestinal epithelium (MIR31 conditional knockouts) were given dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS) to induce colitis. We performed chromatin immunoprecipitation and luciferase assays to study proteins that regulate expression of MIR31, including STAT3 and p65, in LOVO colorectal cancer cells and organoids derived from mouse colon cells. Partially hydrolyzed alpha-lactalbumin was used to generate peptosome nanoparticles, and MIR31 mimics were loaded onto their surface using electrostatic adsorption. Peptosome–MIR31 mimic particles were encapsulated into oxidized konjac glucomannan (OKGM) microspheres, which were administered by enema into the large intestines of mice with DSS-induced colitis. Intestinal tissues were collected and analyzed by histology and immunohistochemistry.ResultsLevels of MIR31 were increased in inflamed mucosa from patients with CD or UC, and from mice with colitis, compared with controls. STAT3 and nuclear factor-κB activated transcription of MIR31 in colorectal cancer cells and organoids in response to tumor necrosis factor and interleukin (IL)6. MIR31-knockout and conditional-knockout mice developed more severe colitis in response to DSS and TNBS, with increased immune responses, compared with control mice. MIR31 bound to 3ʹ untranslated regions of Il17ra and Il7r messenger RNAs (RNAs) (which encode receptors for the inflammatory cytokines IL17 and IL7) and Il6st mRNA (which encodes GP130, a cytokine signaling protein). These mRNAs and proteins were greater in MIR31-knockout mice with colitis, compared with control mice; MIR31 and MIR31 mimics inhibited their expression. MIR31 also promoted epithelial regeneration by regulating the WNT and Hippo signaling pathways. OKGM peptosome–MIR31 mimic microspheres localized to colonic epithelial cells in mice with colitis; they reduced the inflammatory response, increased body weight and colon length, and promoted epithelial cell proliferation.ConclusionsMIR31, increased in colon tissues from patients with CD or UC, reduces the inflammatory response in colon epithelium of mice by preventing expression of inflammatory cytokine receptors (Il7R and Il17RA) and signaling proteins (GP130). MIR31 also regulates the WNT and Hippo signaling pathways to promote epithelial regeneration following injury. OKGM peptosome–MIR31 microspheres localize to the colon epithelium of mice to reduce features of colitis. Transcript Profiling: GSE123556 Levels of microRNA 31 (MIR31) are increased in intestinal tissues from patients with inflammatory bowel diseases and colitis-associated neoplasias. We investigated the effects of this microRNA on intestinal inflammation by studying mice with colitis. We obtained colon biopsy samples from 82 patients with ulcerative colitis (UC), 79 patients with Crohn’s disease (CD), and 34 healthy individuals (controls) at Shanghai Tenth People’s Hospital. MIR31- knockout mice and mice with conditional disruption of Mir31 specifically in the intestinal epithelium (MIR31 conditional knockouts) were given dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS) to induce colitis. We performed chromatin immunoprecipitation and luciferase assays to study proteins that regulate expression of MIR31, including STAT3 and p65, in LOVO colorectal cancer cells and organoids derived from mouse colon cells. Partially hydrolyzed alpha-lactalbumin was used to generate peptosome nanoparticles, and MIR31 mimics were loaded onto their surface using electrostatic adsorption. Peptosome–MIR31 mimic particles were encapsulated into oxidized konjac glucomannan (OKGM) microspheres, which were administered by enema into the large intestines of mice with DSS-induced colitis. Intestinal tissues were collected and analyzed by histology and immunohistochemistry. Levels of MIR31 were increased in inflamed mucosa from patients with CD or UC, and from mice with colitis, compared with controls. STAT3 and nuclear factor-κB activated transcription of MIR31 in colorectal cancer cells and organoids in response to tumor necrosis factor and interleukin (IL)6. MIR31-knockout and conditional-knockout mice developed more severe colitis in response to DSS and TNBS, with increased immune responses, compared with control mice. MIR31 bound to 3ʹ untranslated regions of Il17ra and Il7r messenger RNAs (RNAs) (which encode receptors for the inflammatory cytokines IL17 and IL7) and Il6st mRNA (which encodes GP130, a cytokine signaling protein). These mRNAs and proteins were greater in MIR31-knockout mice with colitis, compared with control mice; MIR31 and MIR31 mimics inhibited their expression. MIR31 also promoted epithelial regeneration by regulating the WNT and Hippo signaling pathways. OKGM peptosome–MIR31 mimic microspheres localized to colonic epithelial cells in mice with colitis; they reduced the inflammatory response, increased body weight and colon length, and promoted epithelial cell proliferation. MIR31, increased in colon tissues from patients with CD or UC, reduces the inflammatory response in colon epithelium of mice by preventing expression of inflammatory cytokine receptors (Il7R and Il17RA) and signaling proteins (GP130). MIR31 also regulates the WNT and Hippo signaling pathways to promote epithelial regeneration following injury. OKGM peptosome–MIR31 microspheres localize to the colon epithelium of mice to reduce features of colitis. Transcript Profiling: GSE123556" @default.
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• W2911247714 date "2019-06-01" @default.
• W2911247714 modified "2023-10-18" @default.
• W2911247714 title "MicroRNA-31 Reduces Inflammatory Signaling and Promotes Regeneration in Colon Epithelium, and Delivery of Mimics in Microspheres Reduces Colitis in Mice" @default.
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• W2911247714 cites W1993677820 @default.
• W2911247714 cites W1996583924 @default.
• W2911247714 cites W1997888176 @default.
• W2911247714 cites W2001709426 @default.
• W2911247714 cites W2008755438 @default.
• W2911247714 cites W2017995578 @default.
• W2911247714 cites W2024346860 @default.
• W2911247714 cites W2032175829 @default.
• W2911247714 cites W2053714569 @default.
• W2911247714 cites W2067568195 @default.
• W2911247714 cites W2070715537 @default.
• W2911247714 cites W2074254007 @default.
• W2911247714 cites W2081375829 @default.
• W2911247714 cites W2086907971 @default.
• W2911247714 cites W2087679721 @default.
• W2911247714 cites W2091764094 @default.
• W2911247714 cites W2109838283 @default.
• W2911247714 cites W2117077782 @default.
• W2911247714 cites W2117765445 @default.
• W2911247714 cites W2121159565 @default.
• W2911247714 cites W2122364696 @default.
• W2911247714 cites W2131698002 @default.
• W2911247714 cites W2176271034 @default.
• W2911247714 cites W2220188867 @default.
• W2911247714 cites W2301342743 @default.
• W2911247714 cites W2321738099 @default.
• W2911247714 cites W2557502945 @default.
• W2911247714 cites W2563393060 @default.
• W2911247714 cites W2592596430 @default.
• W2911247714 cites W2599036809 @default.
• W2911247714 cites W2601678568 @default.
• W2911247714 cites W2620756707 @default.
• W2911247714 cites W2753494459 @default.
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• W2911247714 cites W2770048197 @default.
• W2911247714 cites W2793011044 @default.
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• W2911247714 doi "https://doi.org/10.1053/j.gastro.2019.02.023" @default.
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