The HO-1-expressing bone mesenchymal stem cells protects intestine from ischemia and reperfusion injury

Yan, Xuetao; Cheng, Xiaoli; He, Xiang-Hu; Zheng, Wenzhong; Yuan, Xiaoyi; Hu, Chen

doi:10.1186/s12876-019-1042-9

Cited by 12 publications

(8 citation statements)

References 24 publications

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“…There is evidence that depletion of Nrf2 increases susceptibility to liver injury [28], indicating that Nrf2 plays a major role in the hepatic protective pathway. HO-1 is a stress-induced isoform that attenuates oxidative damage, and previous studies have reported that HO-1 protects against liver, neurological, renal, and intestinal IRI [29,30]. These studies have shown that miR-141-3p regulates oxidative stress by targeting Keap1.…”

Section: Discussionmentioning

confidence: 83%

MicroRNA-141-3p Attenuates Oxidative Stress-induced Hepatic Ischemia Reperfusion Injury via Keap1/Nrf2 Pathway

Chen

Dai

et al. 2021

Preprint

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Hepatic ischemia reperfusion injury (IRI) is a major factor affecting the prognosis of liver transplantation through a series of severe cell death and inflammatory responses. MicroRNA-141-3p (miR-141-3p) has been reported to be associated with hepatic steatosis and other liver diseases. However, the potential role of miR-141-3p in hepatic IRI is currently unknown. In the present study, we found that miR-141-3p levels were negatively correlated with alanine aminotransferase (ALT)/aspartate aminotransferase (AST) in liver transplantation patients. The results demonstrated that miR-141-3p was decreased in mouse liver tissue after hepatic IRI in mice and in hepatocytes after hypoxia/reoxygenation (H/R). Overexpression of miR-141-3p directly decreased Kelch-like ECH-associated protein 1 (Keap1) levels and attenuated cell apoptosis in vivo and in vitro, while inhibition of miR-141-3p facilitated apoptosis. Further experiments revealed that overexpression of miR-141-3p also attenuated oxidative stress-induced damage in hepatocytes under H/R conditions. Taken together, our results indicate that miR-141-3p plays a major role in hepatic IRI through the Keap1 signaling pathway, and the present study suggests that miR-141-3p might have a protective effect on hepatic IRI to some extent.

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Section: Discussionmentioning

confidence: 83%

MicroRNA-141-3p Attenuates Oxidative Stress-induced Hepatic Ischemia Reperfusion Injury via Keap1/Nrf2 Pathway

Chen

Dai

et al. 2021

Preprint

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“…In rats subjected to 45 min of the celiac trunk and superior mesenteric artery ischemia, followed by 60 min of reperfusion, treatment with melatonin (applied 5 min before to reperfusion) significantly reduced ischemia-reperfusion injury (neutrophil-mediated oxidative stress) as indicated by the inhibition of pathways related to ONOO − measured by the molecular probe DHR123 [75]. Yan et al used the DCFH-DA fluorescent probe to confirm the attenuation of oxidative stress induced by temporary ischemia of the superior mesenteric artery in mice treated with HO-1-expressing bone mesenchymal stromal cells (BMSC); based on the analysis using the fluorescent probe, it was concluded that BMSC that express HO-1 are more effective than treatment with BMSC alone in limiting intestinal damage and inflammation following ischemia and reperfusion injury [76]. Nagira et al used DHR123 in the monolayers of human intestinal epithelial cell line to indicate that tight junctions and dysfunction of P-glycoprotein are induced through generation of reactive oxygen metabolites by ischemia and reperfusion in vitro model, and demonstrate the use of lutein as an antioxidant [77].…”

Section: Translational Studiesmentioning

confidence: 99%

Translational Application of Fluorescent Molecular Probes for the Detection of Reactive Oxygen and Nitrogen Species Associated with Intestinal Reperfusion Injury

et al. 2021

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Acute mesenteric ischemia, caused by an abrupt interruption of blood flow in the mesenteric vessels, is associated with high mortality. When treated with surgical interventions or drugs to re-open the vascular lumen, the reperfusion process itself can inflict damage to the intestinal wall. Ischemia and reperfusion injury comprise complex mechanisms involving disarrangement of the splanchnic microcirculatory flow and impairment of the mitochondrial respiratory chain due to initial hypoxemia and subsequent oxidative stress during the reperfusion phase. This pathophysiologic process results in the production of large amounts of reactive oxygen (ROS) and nitrogen (RNS) species, which damage deoxyribonucleic acid, protein, lipids, and carbohydrates by autophagy, mitoptosis, necrosis, necroptosis, and apoptosis. Fluorescence-based systems using molecular probes have emerged as highly effective tools to monitor the concentrations and locations of these often short-lived ROS and RNS. The timely and accurate detection of both ROS and RNS by such an approach would help to identify early injury events associated with ischemia and reperfusion and increase overall clinical diagnostic sensitivity. This abstract describes the pathophysiology of intestinal ischemia and reperfusion and the early biological laboratory diagnosis using fluorescent molecular probes anticipating clinical decisions in the face of an extremely morbid disease.

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“…In addition, some studies found that the reduction of human bone MSCs can reduce the intestinal I/R injury mortality [33], and that human umbilical MSCs can provide an intestinal protective effect through nitric oxide dependent pathways [34]. Furthermore, studies have found that melatonin-supported adipose-derived MSCs [35], synergetic application of electroacupuncture and MSCs[36], HO-1-expressing BM-MSCs [37], IL-1β-activated adiposederived MSCs [38], and IL-37 gene-modi ed MSCs also have a protective effect against intestinal I/R injury [39].…”

Section: Introductionmentioning

confidence: 99%

Mesenchymal Stem Cells for the Treatment of Intestinal Ischemia-reperfusion Injury: a Protocol of Systematic Review and Meta-analysis of Animal Models

Zhang

Suo²,

Liu

et al. 2021

Preprint

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Introduction: Intestinal ischemia-reperfusion (I/R) injury is a common clinical event. Mesenchymal stem cells (MSCs) have been widely used to repair intestinal injury in animal models. However, the effects of MSCs on intestinal I/R injury therapy remain unclear. Thus, we will perform a systematic review and meta-analysis of controlled trials to evaluate the efficacy of MSCs in animal models of intestinal I/R injury.Methods and analysis: We will search PubMed, Web of Science, Embase, Cochrane Library, Science Citation Index, China National Knowledge Information database, Wanfang Database, and the Chinese Scientific and Technological Journal Database in May 2021. We will include studies that evaluate the two different interventions for target MSCs to be maintained for the degree of histopathologic changes, mortality rate of rats, tumour necrosis factor α, and diamine oxidase. Two reviewers will independently screen titles and abstracts, perform a full article review, and extract study data. We will also use the SYRCLE tool to assess the risk of bias in the included studies. Furthermore, a random-effects meta-analysis will be conducted. Dichotomous and continuous outcomes will be analysed using risk ratios with 95% confidence intervals (CIs) and weighted mean difference with 95% CIs, respectively. For outcomes where different scales or different measurement methods have been used, the standardised mean difference will be applied. Subgroup and sensitivity analyses will be performed to explore the heterogeneity. Stata (version 12.0, Stata Corp, College Station, Texas, USA) will be used to analyse and pool the individual research results.Ethics and dissemination: This systematic review and meta-analysis does not require an ethical approval because no human beings are involved. We aim to publish this systematic review in a peer-reviewed journal.PROSPERO registration number: CRD42021231826

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The HO-1-expressing bone mesenchymal stem cells protects intestine from ischemia and reperfusion injury

Cited by 12 publications

References 24 publications

MicroRNA-141-3p Attenuates Oxidative Stress-induced Hepatic Ischemia Reperfusion Injury via Keap1/Nrf2 Pathway

MicroRNA-141-3p Attenuates Oxidative Stress-induced Hepatic Ischemia Reperfusion Injury via Keap1/Nrf2 Pathway

Translational Application of Fluorescent Molecular Probes for the Detection of Reactive Oxygen and Nitrogen Species Associated with Intestinal Reperfusion Injury

Mesenchymal Stem Cells for the Treatment of Intestinal Ischemia-reperfusion Injury: a Protocol of Systematic Review and Meta-analysis of Animal Models

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