Role of regenerating gene I in claudin expression and barrier function in the small intestine

Kitayama, Yoshitaka; Fukui, Hirokazu; Hara, Ken; Eda, Hirotsugu; Kodani, Mio; Yang, Mo; Sun, Chao; Yamagishi, Hidetsugu; Tomita, Toshihiko; Oshima, Tadayuki; Watari, Jiro; Takasawa, Shin; Miwa, Hiroto

doi:10.1016/j.trsl.2016.03.007

Cited by 17 publications

(14 citation statements)

References 27 publications

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“…Proteins were extracted from whole colonic tissue as described previously [ 24 ]. The protein extract (30 µg) was fractionated by sodium dodecyl sulfate polyacrylamide gel electrophoresis and transferred to a polyvinylidene difluoride membrane.…”

Section: Methodsmentioning

confidence: 99%

“…Electrical resistance across the stratified epithelium was measured using a Millicell-ERS-2 instrument (Millipore, Bedford, MA, USA) with “chopstick’’ electrodes, as described previously [ 24 ]. The value obtained from a blank insert was subtracted to give the net resistance, which was then multiplied by the membrane area to give the resistance in area-corrected units (Ω·cm 2 ).…”

Section: Methodsmentioning

confidence: 99%

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Alteration of Colonic Mucosal Permeability during Antibiotic-Induced Dysbiosis

Ran

Fukui

et al. 2020

IJMS

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Although dysbiosis is likely to disturb the mucosal barrier system, the mechanism involved has remained unclear. Here, we investigated alterations of colonic mucosal permeability and tight junction (TJ) molecules in mice with antibiotic-induced dysbiosis. Mice were orally administered vancomycin or polymyxin B for 7 days, and then fecal samples were subjected to microbial 16S rRNA analysis. The colonic mucosal permeability was evaluated by chamber assay. The colonic expression of TJ molecules and cytokines was examined by real-time RT-PCR, Western blotting, and immunohistochemistry. Caco2 cells were stimulated with cytokines and their transepithelial electric resistance (TEER) was measured. Vancomycin-treated mice showed significantly lower gut microbiota diversity than controls, and the same tendency was evident in polymyxin B-treated mice. The colonic mucosal permeability was significantly elevated in both vancomycin- and polymyxin B-treated mice. The expression of claudin 4 in the colonic mucosa was decreased in both vancomycin- and polymyxin B-treated mice. Colonic expression of TNF-α and/or IFN-γ was significantly increased in mice that had been administered antibiotics. TNF-α and IFN-γ stimulation dose-dependently decreased TEER in Caco2 cells. Antibiotic-induced dysbiosis is correlated with the enhancement in colonic tissue permeability, accompanied by a reduction in claudin 4 expression and enhancement in TNF-α and/or IFN-γ expression in mice.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Alteration of Colonic Mucosal Permeability during Antibiotic-Induced Dysbiosis

Ran

Fukui

et al. 2020

IJMS

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“…Immunohistochemical staining for the mannose receptor (MR; a marker of M2-polarized macrophages) and tryptase (a marker of mast cells) was performed using an Envision kit (Dako; Agilent Technologies, Inc., Santa Clara, CA, USA) as described previously ( 16 ). The primary antibodies applied were: anti-MR (dilution 1:5,000; cat.…”

Section: Methodsmentioning

confidence: 99%

Association between gastrointestinal motility and macrophage/mast cell distribution in mice during the healing stage after DSS‑induced colitis

et al. 2018

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Irritable bowel syndrome (IBS) frequently occurs after infectious colitis or inflammatory bowel disease in patients with complete remission. This suggests that post-inflammation-associated factors may serve a role in the pathophysiology of IBS; however, the mechanism responsible remains unclear. In the present study, the involvement of macrophages and mast cells in alteration of gastrointestinal (GI) motility was investigated in mice in the remission stage after acute colitis. C57BL/6 mice were administered 2% dextran sulfate sodium in drinking water for 5 days and their intestinal tissues were investigated at intervals for up to 24 weeks. Expression of the mannose receptor (MR) and tryptase was examined by immunohistochemistry, and the GI transit time (GITT) was measured by administration of carmine red solution. A minimal degree of inflammatory cell infiltration persisted in the colon and also the small intestine of mice in remission after colitis and the GITT was significantly shorter. The number of muscularis MR-positive macrophages was significantly increased in the small intestine of mice in remission after colitis and negatively correlated with GITT. Furthermore, results indicated that the number of muscularis tryptase-positive mast cells was significantly increased throughout the intestine of mice during the healing process after colitis and was positively correlated with GITT. The present findings suggested an increased number of macrophages and/or mast cells in the intestinal muscular layer may be associated with the pathophysiology of GI dysmotility after colitis.

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“…After establishing sepsis, gavage with 4000 Da FITC-dextran (600 mg/kg body weight, 80 mg/mL in phosphate-buffered saline, Sigma-Aldrich, St. Louis, MO, USA) was performed, and blood sample was collected after 1 h. The plasma FITCdextran concentration was determined using a fluorescence spectrophotometer at an emission wavelength of 520 nm [17][18][19]. FITC-dextran infiltration in the tissue was further observed by fluorescence microscopy (EVOS FL, Life Technologies, Carlsbad, CA, USA).…”

Section: Detection Of Intestinal Permeability Using Fitc-dextranmentioning

confidence: 99%

ADAR1 Alleviates Inflammation in a Murine Sepsis Model via the ADAR1-miR-30a-SOCS3 Axis

Zhou

Liu

Zhao

et al. 2020

Mediators of Inflammation

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Adenosine deaminase acting on double-stranded RNA 1 (ADAR1) mediates adenosine-to-inosine (A-to-I) RNA editing events. ADAR1 is highly expressed in “septic” macrophages and in small intestinal tissues of mice with sepsis. Overexpression of ADAR1 suppresses inflammation and intestinal damage. However, the specific underlying mechanism is unclear. This study was conducted to explore how microRNA (miRNA) regulates the anti-inflammatory mechanism of macrophages following ADAR1 upregulation. A murine sepsis model was established by cecal ligation and puncture (CLP). Mice were randomly assigned to sham, CLP, and CLP+ADAR1 groups. Hematoxylin and eosin (HE) staining and fluorescence isothiocyanate-dextran were used to evaluate intestinal injury and permeability. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blotting, and Luminex assays were performed to detect changes in the expression of inflammatory cytokines. Adenoviruses were used to express ADAR1 in RAW 264.7 cells. Ribonucleoprotein immunoprecipitation analysis was conducted to detect the binding of ADAR1 and miRNAs. A dual-luciferase reporter assay was used to detect the binding of miRNAs and regulatory factors. We observed that ADAR1 significantly increased the expression of suppressor of cytokine signaling 3 (SOCS3) in macrophages and reduced the expression of interleukin-6 in macrophages and the serum, thereby reducing intestinal permeability and mucosal injury in mice with sepsis. The RNA-ribonucleoprotein immunoprecipitation binding assay and qRT-PCR demonstrated a direct interaction between ADAR1 and pri-miR-30a. The luciferase assay demonstrated that SOCS3 was significantly inhibited by miR-30a-5p, the mature product of miR-30a. Thus, ADAR1 exerts a protective effect against sepsis by reducing inflammation and organ damage via the ADAR1-miR-30a-SOCS3 axis.

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Role of regenerating gene I in claudin expression and barrier function in the small intestine

Cited by 17 publications

References 27 publications

Alteration of Colonic Mucosal Permeability during Antibiotic-Induced Dysbiosis

Alteration of Colonic Mucosal Permeability during Antibiotic-Induced Dysbiosis

Association between gastrointestinal motility and macrophage/mast cell distribution in mice during the healing stage after DSS‑induced colitis

ADAR1 Alleviates Inflammation in a Murine Sepsis Model via the ADAR1-miR-30a-SOCS3 Axis

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