Detection of the MicroRNA Expression Profile in Skeletal Muscles of Burn Trauma at the Early Stage in Rats

Chai, Jiake

doi:10.5505/tjtes.2015.80707

Cited by 4 publications

(4 citation statements)

References 22 publications

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“…Since the conservation of miRNA sequences between species is high, these miRNAs have potential as biomarkers for human stroke. Some of the blood miRNAs found in rat models were previously reported in brain, hyperoxia, or stress-related diseases, but not in stroke ( Table S2 ) [ 20 , 21 , 22 , 23 , 24 , 25 ]. In addition, many of the human miRNAs with similar sequences were reported to be related to several diseases, but none was reported to be related to stroke ( Table S3 ) [ 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 ].…”

Section: Discussionmentioning

confidence: 99%

Gene Expression Analysis of the Effect of Ischemic Infarction in Whole Blood

Takuma

Abe

Saito

et al. 2017

IJMS

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Given the abundance of stroke patients and deaths from stroke worldwide, many studies concerning the aftermath of stroke are being carried out. To reveal the precise effect of ischemic infarction, we conducted a comprehensive gene expression analysis. Alongside a middle cerebral artery occlusion (MCAO) Sprague–Dawley rat model, we used a group undergoing sham surgery for comparison, which was the same as MCAO surgery but without blood vessel occlusion. Subsequently, infarction of the brains of MCAO-treated rats occurred, but did not occur in the sham-treated rats. Using whole blood, we carried out DNA microarray analysis, revealing the gene expression alterations caused by stroke. Downregulation of immune pathways and cluster of differentiation (CD) molecules indicated immunodepression. By conducting miRNA microarray analysis, we extracted seven miRNAs as significantly regulated: miR-107-5p, miR-383-5p, miR-24-1-5p, mir-191b, miR-196b-5p, and miR-3552 were upregulated, and mir-194-1 was downregulated. Among these seven miRNAs, three had one target mRNA each that was extracted as differentially expressed, and the expression levels of all pairs were inversely correlated. This indicates the occurrence of miRNA–mRNA regulatory systems in blood: between miR-107-5p and H2A histone family member Z (H2afz), miR-196b-5p and protein tyrosine phosphatase receptor type C (Ptprc), and miR-3552 and serine/arginine-rich splicing factor 2 (Srsf2). Moreover, six miRNAs had matching human miRNAs with similar sequences, which are potential human stroke biomarkers.

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Section: Discussionmentioning

confidence: 99%

Gene Expression Analysis of the Effect of Ischemic Infarction in Whole Blood

Takuma

Abe

Saito

et al. 2017

IJMS

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“…Previous studies have demonstrated that miR-181c plays a potential role in regulating TNF-a expression after ischemia-mediated neuronal injury and hypoxia microglial activation-induced neuroinflammation ( Zhang et al, 2012 , Hutchison et al, 2013 ). We previously compared miRNA expression between severe burn rats and sham rats by miRNA array and found that miR-181c was deregulated in early stage burn rats ( Haijun et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Exosome Derived From Human Umbilical Cord Mesenchymal Stem Cell Mediates MiR-181c Attenuating Burn-induced Excessive Inflammation

et al. 2016

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Mesenchymal stem cell (MSC)-derived exosomes have diverse functions in regulating wound healing and inflammation; however, the molecular mechanism of human umbilical cord MSC (hUCMSC)-derived exosomes in regulating burn-induced inflammation is not well understood. We found that burn injury significantly increased the inflammatory reaction of rats or macrophages exposed to lipopolysaccharide (LPS), increased tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β) levels and decreased IL-10 levels. hUCMSC-exosome administration successfully reversed this reaction. Further studies showed that miR-181c in the exosomes played a pivotal role in regulating inflammation. Compared to control hUCMSC-exosomes, hUCMSC-exosomes overexpressing miR-181c more effectively suppressed the TLR4 signaling pathway and alleviated inflammation in burned rats. Administration of miR-181c-expressing hUCMSC-exosomes or TLR4 knockdown significantly reduced LPS-induced TLR4 expression by macrophages and the inflammatory reaction. In summary, miR-181c expression in hUCMSC-exosomes reduces burn-induced inflammation by downregulating the TLR4 signaling pathway.

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“…Protein translation and degradation are two methods of post-transcription regulation, and miRNAs play a critical role in regulating protein translation. Our previous report indicated that the expression levels of many miRNAs were altered in the tibialis anterior muscles of burn rats and that the expression of miR-628 was significantly increased after burn injury 32 . miR-628 expression levels in the tibialis anterior muscles of sham and burn rats were determined using an miRNA array and are shown in Fig.…”

Section: Resultsmentioning

confidence: 98%

“…Thus, miRNAs play a pivotal role in regulating muscle atrophy. Our previous study showed that there were 4 upregulated miRNAs including miR-628, miR-107, miR-201, and miR-222 in tibialis anterior muscle after burn injury 32 . And IRS1, the critical muscle atrophy-related protein, was the potential target of miR-628.…”

Section: Discussionmentioning

confidence: 98%

miR-628 Promotes Burn-Induced Skeletal Muscle Atrophy via Targeting IRS1

Xiao

Liu

et al. 2016

Int. J. Biol. Sci.

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Skeletal muscle atrophy is a common clinical feature among patients with severe burns. Previous studies have shown that miRNAs play critical roles in the regulation of stress-induced skeletal muscle atrophy. Our previous study showed that burn-induced skeletal muscle atrophy is mediated by miR-628. In this study, compared with sham rats, rats subjected to burn injury exhibited skeletal muscle atrophy, as well as significantly decreased insulin receptor substrate 1 (IRS1) protein expression and significantly increased skeletal muscle cell apoptosis. An miRNA array showed that the levels of miR-628, a potential regulator of IRS1 protein translation, were also clearly elevated. Second, L6 myocyte cell apoptosis increased after induction of miR-628 expression, and IRS1 and p-Akt protein expression decreased significantly. Expression of the cell apoptosis-related proteins FoxO3a and cleaved caspase 3 also increased after induction of miR-628 expression. Finally, forced miR-628 expression in normal rats resulted in increased cell apoptosis and skeletal muscle atrophy, as well as changes in IRS1/Akt/FoxO3a signaling pathway activity consistent with the changes in protein expression described above. Inhibiting cell apoptosis with Z-VAD-FMK resulted in alleviation of burn-induced skeletal muscle atrophy. In general, our results indicate that miR-628 mediates burn-induced skeletal muscle atrophy by regulating the IRS1/Akt/FoxO3a signaling pathway.

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Detection of the MicroRNA Expression Profile in Skeletal Muscles of Burn Trauma at the Early Stage in Rats

Cited by 4 publications

References 22 publications

Gene Expression Analysis of the Effect of Ischemic Infarction in Whole Blood

Gene Expression Analysis of the Effect of Ischemic Infarction in Whole Blood

Exosome Derived From Human Umbilical Cord Mesenchymal Stem Cell Mediates MiR-181c Attenuating Burn-induced Excessive Inflammation

miR-628 Promotes Burn-Induced Skeletal Muscle Atrophy via Targeting IRS1

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