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MiRNA expression profile in intestinal ischemia reperfusion of adult mice

ABSTRACT: 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.

ORGANISM(S): Mus musculus Rattus norvegicus Homo sapiens

PROVIDER: GSE83701 | GEO | 2016/06/25

SECONDARY ACCESSION(S): PRJNA326757

REPOSITORIES: GEO

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miRNA expression profile in intestinal ischemia reperfusion of adult mice

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

Blockade of TNFα after ischemia reperfusion injury ameliorates renal prognosis

Project description:Recently, acute kidney injury (AKI) is thought to develop a predisposition toward chronic kidney disease. But the detailed mechanism of the disease progression after AKI is unknown. We made two ischemia-reperfusion injury (IRI) mice models, repaired kidney model and atrophic kidney model, and studied the mechanism that kidney after IRI became atrophy. We found that the atrophy kidney model had two peaks of apoptosis 3 and 14 days after IRI, whereas the repaired kidney model had only one apoptosis peak 3 days after IRI. We showed that the second apoptosis is responsible for the kidney atrophy. Moreover, apoptotic ligands, TNFα and FasL were upregulated at the same time of two apoptosis peaks on the atrophic kidney, and blockade of them before IRI prevented kidney from falling into atrophy. Surprisingly, inhibition of the second apoptosis by anti-TNFα antibody protected from renal atrophy. We propose that apoptosis might play a major role in AKI progression and blockade of TNFα after IRI will be a new therapeutic approach for AKI.

2012-08-10 | GSE39766 | GEO

Ubc9 overexpression and SUMO1 deficiency blunt inflammation after intestinal ischemia/reperfusion.

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

MicroRNA-802 regulates the innate immune response through Paneth cell expansion and Wnt signaling

Project description:Paneth cells are important for maintaining epithelial cell renewal and modulating innate immune function in the intestine through secretion of growth factors and antimicrobial peptides, which help sustain epithelial stem and progenitor cells and contribute to the intestinal barrier and protection against pathogenic bacteria. Here we show that the intestine-enriched miR-802 is a central regulator of intestinal epithelial cell proliferation and Paneth cell function. Genetic ablation of mir-802 in mice leads to amplified ROS generation and Notch/Wnt signaling, increased intestinal epithelial turnover, impaired enterocyte differentiation and nutrient uptake, and increased enterocyte apoptosis. Mice lacking mir-802 in the intestine also exhibit Paneth cell expansion, increased antimicrobial peptide production, and protection against Salmonella infection. This phenotype relies on the miR-802 target gene Tmed9.

2020-12-11 | GSE148198 | GEO

Pathogenic Natural Antibodies Recognizing Annexin IV Are Required to Develop Intestinal Ischemia-Reperfusion Injury

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

Glutamine attenuates renal ischemia-reperfusion injury and prevents acute kidney damage

Project description:Acute kidney injury (AKI) represents a common complication in critically ill patients that is associated with an increased morbidity and mortality. Currently, no effective treatment options are available. Here, we show that glutamine significantly attenuates leukocyte recruitment and inflammatory signaling in human and murine tubular epithelial cells (TECs). In a murine AKI model induced by ischemia-reperfusion-injury (IRI) we show that glutamine causes transcriptomic and proteomic reprogramming in renal TECs and neutrophils, resulting in decreased epithelial apoptosis, neutrophil recruitment and improved mitochondrial functionality and respiration provoked by an ameliorated oxidative phosphorylation. We identify the proteins glutamine gamma glutamyltransferase 2 (Tgm2) and apoptosis signal-regulating kinase (Ask1) as the major targets of glutamine in apoptotic signaling. Increased Tgm2 expression and reduced Ask1 activation result in decreased JNK activation leading to a diminished mitochondrial intrinsic apoptosis in kidneys upon IRI-induced AKI and under hypoxia or following TNFα-treatment of TECs. Consequently, glutamine administration attenuated kidney injury in vivo during AKI progression as well as TEC viability in vitro under inflammatory and hypoxic conditions.

2023-03-11 | PXD029723 | Pride

Novel role of miR-18a-5p and Galanin in rat lung ischemia-reperfusion mediated response

Project description:Lung ischemia-reperfusion (IR) is known to occur after lung transplantation or cardiac bypass. IR leads to tissue inflammation and damage, is also associated with increased morbidity and mortality. Various receptors are known to partake in activation of innate immune system, but the downstream mechanism of tissue damage and inflammation is yet unknown. MicroRNAs (miRNA) are in the forefront in regulating ischemia reperfusion injury and are involved in inflammatory response. Here, we have identified by high throughput approach and evaluated distinct set of miRNAs that may play a role in response to IR in rat lung tissue. Top three differentially expressed miRNAs were validated through quantitative PCRs in the IR rat lung model and an in vitro model of IR of hypoxia and reoxygenation exposed type II alveolar cells. Among the miRNAs, miR-18a-5p showed consistent downregulation in both the model systems on IR. Cellular and molecular analysis brought to light a crucial role of this miRNA in ischemia reperfusion. MiR-18a-5p plays a role in IR mediated apoptosis, ROS production and regulates the expression of neuropeptide Galanin. It also influences the nuclear localization of transcription factor: Nuclear factor-erythroid 2 related factor (Nrf2) which in turn may regulate the expression of miR-18a gene. Thus, we have not only established a rat model for lung IR and enumerate the important miRNAs involved in IR but have also extensively characterized the role of miR-18a-5p in the same. This study will have important clinical and therapeutic implications for and during transplantation procedures.

2020-11-19 | GSE161520 | GEO

Exosomal circEZH2_005, an intestinal injury biomarker, alleviates intestinal ischemia/reperfusion injury by mediating hnRNPA1/Gprc5a signaling

Project description:Although plasma exosomal circular RNAs (circRNAs) are valuable biomarkers and therapeutic targets for various diseases, their role in intestinal I/R injury remains unknown. This study screens the expression profile of circRNAs in intestinal tissue exosomes collected from intestinal I/R mice.

2023-09-13 | GSE227355 | GEO

Plasma microRNA array analysis following cardiac ischemia-reperfusion (I/R) injury

Project description:In this study, total 68 cardiac diseases-related miRNAs were detected

2015-11-13 | GSE74951 | GEO

Gene expression in intestinal epithelial crypt and villus cell populations

Project description:We analyzed gene expression profiles in isolated mouse LGR5+ intestinal stem cells, lineage-specific enterocyte and secretory progenitors, and terminally differentiated villus enterocytes. Gene Ontology analyses of cell type-specific transcripts indicated their expected biological functions. We hybridized Affmetrix 430A 2.0 mouse microarrays with processed RNA isolated from purified Lgr5+ intestinal stem cells, secretory (Sec-Pro) and enterocyte (Ent-Pro) crypt progenitors, and mature villus enterocytes (ENT).

2014-01-06 | E-GEOD-51398 | biostudies-arrayexpress

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