miR-34a-5p Inhibition Alleviates Intestinal Ischemia/Reperfusion-Induced Reactive Oxygen Species Accumulation and Apoptosis <i>via</i> Activation of SIRT1 Signaling

Wang, Guangzhi; Yao, Jihong; Li, Zhenlu; Zu, Guo; Feng, Decheng; Shan, Wen; Li, Yang; Hu, Yan; Zhao, Yongfu; Tian, Xiaofeng

doi:10.1089/ars.2015.6492

Cited by 109 publications

(95 citation statements)

References 59 publications

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“…Furthermore, miR-34a-5p inhibition protects cardiomyocyte against apoptosis post myocardial infarction via negatively regulating ALDH2 [46]. MiR-34a-5p inhibition alleviates intestinal ischemia/reperfusion-induced reactive oxygen species accumulation and apoptosis via activation of SIRT1 signaling [47]. In addition, miR-146a-5p has a protective effect against cardiac ischemia/hypoxia-induced cardiac dysfunction and apoptosis through the TRAF6-p-p38-caspase-3 signal pathway [48].…”

Section: Discussionmentioning

confidence: 99%

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Zhi

Shao

Xue

et al. 2017

Cell Physiol Biochem

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Background/Aims: Hypoxic/ischemic injury to the liver is a frequently encountered clinical problem with limited therapeutic options. Since microRNAs (miRNAs) are involved in hypoxic/ ischemic events, and δ-opioid receptor (DOR) is protective against hypoxic/ischemic injury, we asked if pharmacological activation of DOR can alter hypoxic events by regulating miRNA expression in the liver. As the first step, the present work aimed at testing the effect of DOR activation on hepatic miRNA expression in hypoxia. Methods: Male Sprague Dawley rats were exposed to hypoxia (9.5-10% O₂) for 1, 5, or 10 days with or without DOR activation. The target miRNAs were selected according to TaqMan low-density array (TLDA) data and analyzed by quantitative real-time PCR. Results: We found that: 1) 1-day hypoxia caused the upregulation of 9 miRNAs (miR-7a-5p, miR-10a-5p, miR-25-3p, miR-26b-5p, miR-122-5p, miR-128a-3p, miR-135b-5p, miR-145-5p, and miR-181a-5p) and the downregulation of 2 miRNAs (miR-34a-5p and miR-182); 2) 5 and 10-days hypoxia altered the expression of 4 miRNAs (miR-34c-5p, miR-184, miR-107-3p and miR192-5p); 3) DOR activation shifted the expression of 8 miRNAs (miR-122-5p, miR-146a-5p, miR-30e-5p, miR-128a-3p, miR-182, miR-192-5p miR-107-3p and miR-184) in normoxic condition; and 4) DOR activation modified hypoxia-induced changes in 6 miRNAs (miR-142-5p, miR-145-5p, miR-146a-5p, miR-204-5p, miR-34a-5p and miR-192-5p). Conclusion: Hypoxia significantly modifies the miRNA profile in the liver, while DOR activation can modify the hypoxic modification. Therefore, it is potentially possible to alter hypoxic/ischemic pathophysiology in the liver through DOR pharmacotherapy.

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Section: Discussionmentioning

confidence: 99%

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Zhi

Shao

Xue

et al. 2017

Cell Physiol Biochem

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“…In our opinion, such a genetic profile is adaptive in nature and aimed at mobilizing intrinsic resources to reduce the destruction. In I/R injury, activation of apoptosis has been demonstrated for the intestinal tissue [Yang et al, 2013;Wang et al, 2016] and in cultured endothelial cells [Yang et al, 2009]. Thus, it can be assumed that the development of injury in our working model is characterized by the activation of common cell death pathways.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, it can be assumed that the development of injury in our working model is characterized by the activation of common cell death pathways. A key factor for the increase in apoptosis-related gene expression is oxidative stress [Wang et al, 2016].…”

Section: Discussionmentioning

confidence: 99%

Vascular Pathology of Ischemia/Reperfusion Injury of Rat Small Intestine

Gordeeva

Шарапов²,

Tikhonova³

et al. 2017

Cells Tissues Organs

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Ischemia/reperfusion (I/R) injury of the small intestine caused by occlusion of the superior mesenteric artery affects the intestinal tissue as well as components of the blood circulatory system from the microvasculature to mesenteric vessels. The aim of this work was to study the correlation between the dynamics of destruction development in the intestinal tissue, microvasculature, and mesenteric vessels in I/R of the small intestine. The microvasculature was analyzed by whole-organ continuous monitoring of the intestinal mucosal blood perfusion by laser Doppler flowmetry during the entire I/R. Real-time RT-PCR was used to assess gene expression of NF-κB, caspase-3, Ki67, and TNF-α in blood vessels. At the start of reperfusion, the first targets to be disrupted are microvessels in the apical villi. Injury of the apical part of the microcirculatory bloodstream correlates with the reduction in intestinal mucosal blood perfusion, which occurred simultaneously with apical villous destruction. By the end of the reperfusion period, the low intestinal mucosal blood perfusion is mirrored by the destruction of the microvasculature and mucosal structures in the entire organ. The development of mesenteric vessel injury is characterized by a change in NO metabolism and damaged endothelial cells concomitant with an alteration in the expression of genes encoding NF-κB, caspase-3, and Ki67 by the end of the reperfusion period. In I/R injury, detrimental effects on the intestinal tissue, microvasculature, and mesenteric vessels develop and exhibit common mechanisms of function, which show strong correlations.

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“…An intestinal I/R model was established by superior mesenteric artery (SMA) occlusion as described previously by us [23]. Briefly, all the mice were anesthetized by an intraperitoneal injection of pentobarbital (50 mg/kg body weight).…”

Section: Intestinal I/r Model Construction and Ipoc Treatmentmentioning

confidence: 99%

Microarray Analysis of Differentially Expressed Profiles of Circular RNAs in a Mouse Model of Intestinal Ischemia/Reperfusion Injury with and Without Ischemic Postconditioning

Feng

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Ischemic postconditioning (iPoC) represents a promising strategy to mitigate ischemia/reperfusion (I/R) injury of the intestine, yet the mechanisms of this treatment remain to be elucidated. Circular RNAs (circRNAs), a novel class of endogenous non-coding RNAs, have recently been recognized as important regulators of gene expression and pathological processes. Here, we aimed to investigate the expression patterns of circRNAs after intestinal I/R with and without iPoC and, furthermore, to explore the potential mechanisms of iPoC in relation to the differentially expressed circRNAs. Methods: The global circRNA and mRNA expression profiles in mouse intestinal mucosa were initially screened by microarray (n = 3 per group) and quantitative real-time PCR was used to validate the expression pattern of circRNAs and mRNAs. Bioinformatics analysis including Gene ontology, KEGG pathway analysis, microRNA binding sites identification and circRNA-miRNA-mRNA network construction were utilized for in-depth mechanism exploration. Results: There were 4 up- and 58 downregulated circRNAs as well as 322 up- and 199 downregulated mRNAs in the intestinal I/R group compared with the sham group, whereas compared with I/R, iPoC treatment significantly upregulated 12 circRNAs and 129 mRNAs and downregulated 21 circRNAs and 174 mRNAs. The expression levels of a randomly selected set of 6 circRNAs and 5 mRNAs were successfully validated by qRT-PCR. Through a systematic comparison of the direction of circRNA expression changes in all groups, we identified two circRNAs, circRNA_012412 and circRNA_016863, that may be closely associated with the protective mechanisms of iPoC. Finally, four possible circRNA_012412/circRNA_016863-miRNA-mRNA pathways were predicted, which may play important roles in endogenous protective signaling in iPoC. Conclusions: This study was the first to comprehensively delineate the expression profiles of circRNAs in a mouse model of intestinal I/R and iPoC and provides novel clues for understanding the mechanisms of iPoC against intestinal I/R injury.

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miR-34a-5p Inhibition Alleviates Intestinal Ischemia/Reperfusion-Induced Reactive Oxygen Species Accumulation and Apoptosis via Activation of SIRT1 Signaling

Abstract: miR-34a-5p knockdown attenuates intestinal I/R injury through promoting SIRT1-mediated suppression of epithelial ROS accumulation and apoptosis. This may represent a novel prophylactic approach to intestinal I/R injury. Antioxid. Redox Signal. 24, 961-973.

Cited by 109 publications

References 59 publications

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Vascular Pathology of Ischemia/Reperfusion Injury of Rat Small Intestine

Microarray Analysis of Differentially Expressed Profiles of Circular RNAs in a Mouse Model of Intestinal Ischemia/Reperfusion Injury with and Without Ischemic Postconditioning

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