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MicroRNA Profiling in Ischemia-Reperfusion Injury of the Gracilis Muscle in Rats

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE21423 | GEO | 2010/04/22

SECONDARY ACCESSION(S): PRJNA126375

REPOSITORIES: GEO

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MicroRNA Profiling in Ischemia-Reperfusion Injury of the Gracilis Muscle in Rats

Project description:This SuperSeries is composed of the following subset Series: GSE21405: MicroRNA Profiling In Ischemia-Reperfusion Injury Of The Gracilis Muscle In Rats GSE21406: Potential Target Genes of MicroRNA-21 In Ischemia-Reperfusion Injury Of The Gracilis Muscle In Rats Refer to individual Series

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MicroRNA Profiling in Ischemia-Reperfusion Injury of the Gracilis Muscle in Rats (miRNA data)

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MicroRNA Profiling in Ischemia-Reperfusion Injury of the Gracilis Muscle in Rats (miRNA data)

Project description:Profile the microRNA expression in the Gracilis muscle of rat after 4h ischemia and 24 h reperfusion Following 4 h of ischemia and subsequent reperfusion for 4 h of the gracilis muscles, the specimens were analyzed with an Agilent rat miRNA array to detect the expressed miRNAs in the experimental muscles compared to those from the sham-operated controls. Two-condition experiment, Gracilis muscle after 4h ischemia and reperfusion injury for 24 h v.s. Gracilis muscle (sham control), Biological replicates: 2 control replicates, 2 experiement replicates

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Project description:Transcriptional profiling of rat gracilis muscle after ischemia 4h and reperfusion for 1d, 3d, 7d and 14d v.s. sham control, and correlate the downregulated transcripts to the computational predicted gene targets of ron-miR-21 Following 4 h of ischemia and subsequent reperfusion for 4 h of the gracilis muscles, three miRNAs (miR-21, miR-200c, and miR-205) of 350 tested rat miRNAs were found to have an increased expression in the miRNA array.The expression of the mRNA in the muscle specimens after 4 h of ischemia and reperfusion for 1, 3, 7, and 14 d were detected with the Agilent Whole Rat Genome 4 Ã 44 k oligo microarray. A combined approach using a computational prediction algorithm that included miRanda, PicTar, TargetScanS, MirTarget2, RNAhybrid, and the whole genome microarray experiment was performed by monitoring the mRNA:miRNA association to identify potential target genes. Four-condition experiment, Gracilis muscle after ischemia-reperfusion injury for 1d, 3d, 7d and 14d v.s.Gracilis muscle (sham control), Biological replicates: 1 control replicate, 1 experiement replicate (each condition).

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Vagus Nerve Stimulation Attenuates Acute Skeletal Muscle Injury Induced by Hepatic Ischemia/Reperfusion Injury in Rats.

Project description:Vagus nerve stimulation (VNS) has a protective effect on distal organ injury after ischemia/reperfusion (I/R) injury. We aimed to investigate the protective efficacy of VNS on hepatic I/R injury-induced acute skeletal muscle injury and explore its underlying mechanisms. To test this hypothesis, male Sprague-Dawley rats were randomly divided into three groups: sham group (sham operation, n = 6); I/R group (hepatic I/R with sham VNS, n = 6); and VNS group (hepatic I/R with VNS, n = 6). A hepatic I/R injury model was prepared by inducing hepatic ischemia for 1 h (70%) followed by hepatic reperfusion for 6 h. VNS was performed during the entire hepatic I/R process. Tissue and blood samples were collected at the end of the experiment for biochemical assays, molecular biological preparations, and histological examination. Our results showed that throughout the hepatic I/R process, VNS significantly reduced inflammation, oxidative stress, and apoptosis, while significantly increasing the protein levels of silent information regulator 1 (SIRT1) and decreasing the levels of acetylated forkhead box O1 and Ac-p53, in the skeletal muscle. These data suggest that VNS can alleviate hepatic I/R injury-induced acute skeletal muscle injury by suppressing inflammation, oxidative stress, and apoptosis, potentially via the SIRT1 pathway.

| S-EPMC8762262 | biostudies-literature

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