Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA379474 | ENA |
REPOSITORIES: ENA
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Project description:The intestinal epithelium constitutes a crucial defense to the potentially life-threatening effects of gut microbiota. However, due to a complex underlying vasculature, hypoperfusion and resultant tissue ischemia pose a particular risk to function and integrity of the epithelium. The small ubiquitin-like modifier (SUMO) conjugation pathway critically regulates adaptive responses to metabolic stress and is of particular significance in the gut, as inducible knockout of the SUMO-conjugating enzyme Ubc9 results in rapid intestinal epithelial disintegration. Here we analyzed the pattern of individual SUMO isoforms in intestinal epithelium and investigated their roles in intestinal ischemia/reperfusion (I/R) damage. Immunostaining revealed that epithelial SUMO2/3 expression was almost exclusively limited to crypt epithelial nuclei in unchallenged mice. However, intestinal I/R or overexpression of Ubc9 caused a remarkable enhancement of epithelial SUMO2/3 staining along the crypt-villus axis. Unexpectedly, a similar pattern was found in SUMO1 knockout mice. Ubc9 transgenic mice, but also SUMO1 knockout mice were protected from I/R injury as evidenced by better preserved barrier function and blunted inflammatory responses. PCR array analysis of microdissected villus-tip epithelia revealed a specific epithelial contribution to reduced inflammatory responses in Ubc9 transgenic mice, as key chemotactic signaling molecules such as IL17A were significantly downregulated. Together, our data indicate a critical role particularly of the SUMO2/3 isoforms in modulating responses to I/R and provide the first evidence that SUMO1 deletion activates a compensatory process that protects from ischemic damage.
2018-11-07 | GSE96733 | GEO
Project description:Intestinal ischemia/reperfusion (I/R) contributes to tissue damage, cellular apoptosis, systemic inflammatory responses, and even multiple organ dysfunction syndrome, however, underlying mechanisms remain unkown. In this report, we provide a comprehensive assessment of the expression of 1177 miRNAs on intestine tissues from mice suffering from sham and intestinal I/R. We find that 57 miRNA are up-regulated and 74 are down-regulated significantly. MiRNAs may be integral modulators of intestinal inflammation and enterocyte apoptosis associated with I/R and represent novel targets for future therapeutics. In the study, we profiled miRNA expression in the intestine from mice of 3 sham group and 3 intestinal ischemia/reperfusion group.
2016-06-25 | E-GEOD-83701 | biostudies-arrayexpress
Project description:miRNA expression profile in intestinal ischemia reperfusion of adult mice
| PRJNA326757 | ENA
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Intestinal ischemia-reperfusion (IR) injury is initiated when natural IgM antibodies recognize neo-epitopes that are revealed on ischemic cells. The target molecules and mechanisms whereby these neo-epitopes become accessible to recognition are not well understood. Proposing that isolated intestinal epithelial cells (IEC) may carry IR-related neo-epitopes, we used in vitro IEC binding assays to screen hybridomas created from B cells of unmanipulated wild type C57BL/6 mice. We identified a novel IgM monoclonal antibody (mAb B4) that reacted with the surface of IEC by flow cytometric analysis and was alone capable of causing complement activation, neutrophil recruitment and intestinal injury in otherwise IR-resistant Rag1-/- mice. Monoclonal Ab B4 was found to specifically recognize mouse annexin IV. Pre-injection of recombinant annexin IV blocked IR injury in wild type C57BL/6 mice, demonstrating the requirement for recognition of this protein in order to develop IR injury in the context of a complex natural antibody repertoire. Humans were also found to exhibit IgM natural antibodies that recognize annexin IV. These data in toto identify annexin IV as a key ischemia-related target antigen that is recognized by natural Abs in a pathologic process required in vivo to develop intestinal IR injury. Keywords: Natural antibodies, Annexin, Ischemia Reperfusion, Inflammation, Complement In the study presented here, a total of 4 custom spotted antigen slides were hybridized with known antibodies.
2010-05-05 | E-GEOD-14862 | biostudies-arrayexpress
Project description:STEAP3 alleviates inflammation and fibrosis via iron metabolism in ischemia/reperfusion -associated lung injury (PRJCA038935)
| PRJDB35200 | ENA
Project description:Murine Kidney cells: Control versus Ischemia reperfusion injury
| PRJNA141659 | ENA
Project description: Not available
| S-EPMC11335981 | biostudies-literature
Project description:Validation of Biomarker Expression in Intestinal Ischemia Reperfusion Injury: Insights from Sequencing Data and Experimental Analysis
| PRJNA1040153 | ENA
Project description: Not available
| S-EPMC5321798 | biostudies-literature