MicroRNA-351 inhibits denervation-induced muscle atrophy by targeting TRAF6

He, Qianru; Qiu, Jiaying; Dai, Ming; Fang, Qian; Sun, Xiaoqing; Gong, Yanpei; Ding, Fei; Sun, Hualin

doi:10.3892/etm.2016.3856

Cited by 26 publications

(26 citation statements)

References 28 publications

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“…However, in this study, miR-146a was significantly upregulated by Omp25 or WT B. suis infection in both PAMs and mouse RAW264.7 cells, which suppresses the transcription of TNF-α via targeting TRAF6 and IRAK1. Beside miR-146a, miR-351-5p has also been reported to target TRAF6 to inhibit denervation-induced muscle atrophy ( 41 ). In our work, miR-351-5p was found to be upregulated by Omp25 in RAW264.7 cells to inhibit TNF-α transcription via targeting TRAF6 and IRAK1, yet in PAMs miR-351-5p was not upregulated by Omp25 to regulate TRAF6 and IRAK1.…”

Section: Discussionmentioning

confidence: 99%

Brucella Downregulates Tumor Necrosis Factor-α to Promote Intracellular Survival via Omp25 Regulation of Different MicroRNAs in Porcine and Murine Macrophages

Luo

Zhang

et al. 2018

Front. Immunol.

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Brucella spp. impedes the production of pro-inflammatory cytokines by its outer membrane protein Omp25 in order to promote survival and immune evasion. However, how Omp25 regulates tumor necrosis factor (TNF-α) expression in different mammalian macrophages remains unclear. In this study, we investigated the potential mechanisms by which Omp25 regulates TNF-α expression and found that Omp25-deficient mutant of B. suis exhibited an enhanced TNF-α expression compared with wild-type (WT) B. suis, whereas ectopic expression of Omp25 suppressed LPS-induced TNF-α production at both protein and mRNA levels in porcine alveolar macrophages (PAMs) and murine macrophage RAW264.7 cells. We observed that Omp25 protein as well as WT B. suis upregulated miR-146a, -181a, -181b, and -301a-3p and downregulated TRAF6 and IRAK1 in both PAMs and RAW264.7 cells, but separately upregulates miR-130a-3p in PAMs and miR-351-5p in RAW264.7. The upregulation of miR-146a or miR-351-5p attenuated TNF-α transcription by targeting TRAF6 and IRAK1 at the 3′ untranslated region (UTR), resulting in inhibition of NF-kB pathway, while upregulation of miR-130a-3p, -181a, or -301a-3p correlated temporally with decreased TNF-α by targeting its 3′UTR in PAMs or RAW264.7 cells. In contrast, inhibition of miR-130a-3p, -146a, -181a, and -301a-3p attenuated the inhibitory effects of Omp25 on LPS-induced TNF-α in PAMs, while inhibition of miR-146a, -181a, -301a-3p, and -351-5p attenuated the inhibitory effects of Omp25 in RAW264.7, resulting in an increased TNF-α production and decreased intracellular bacteria in both cells. Taken together, our results demonstrate that Brucella downregulates TNF-α to promote intracellular survival via Omp25 regulation of different microRNAs in porcine and murine macrophages.

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Section: Discussionmentioning

confidence: 99%

Brucella Downregulates Tumor Necrosis Factor-α to Promote Intracellular Survival via Omp25 Regulation of Different MicroRNAs in Porcine and Murine Macrophages

Luo

Zhang

et al. 2018

Front. Immunol.

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“…As early as 2001, two pioneering studies reported that MuRF1 and MAFbx genes were similarly altered in disparate muscle atrophy conditions (Bodine et al, 2001 ; Gomes et al, 2001 ). Among a number of later works, our observations showed that skeletal denervation- or drug-induced skeletal muscle atrophy led to significant up-regulation of MuRF1 and MAFbx (Sun et al, 2014a , b ; He et al, 2016 ), while other researchers found that MuRF1 and MAFbx were up-regulated in skeletal muscle atrophy associated with cancer cachexia and cerebral ischemia (Gomes et al, 2012 ; Desgeorges et al, 2015 ; Winbanks et al, 2016 ).…”

Section: Introductionmentioning

confidence: 86%

“…Briefly, each animal was anesthetized by an intraperitoneal injection of complex narcotics, and the sciatic nerve was exposed through an incision on the lateral aspect of the mid-thigh of the left hind limb. A 1 cm long segment of sciatic nerve was then resected at the site just proximal to the division of tibial and common peroneal nerves, and the incision sites were then closed (Li et al, 2013 ; He et al, 2016 ). Then these animals were performed with daily intraperitoneal injection of saline, PQQ (5 mg/kg) in saline, or NAC (100 mg/Kg) in saline, respectively.…”

Section: Methodsmentioning

confidence: 99%

Mechanistic Role of Reactive Oxygen Species and Therapeutic Potential of Antioxidants in Denervation- or Fasting-Induced Skeletal Muscle Atrophy

Qiu

Fang

et al. 2018

Front. Physiol.

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Skeletal muscle atrophy occurs under various conditions, such as disuse, denervation, fasting, aging, and various diseases. Although the underlying molecular mechanisms are still not fully understood, skeletal muscle atrophy is closely associated with reactive oxygen species (ROS) overproduction. In this study, we aimed to investigate the involvement of ROS in skeletal muscle atrophy from the perspective of gene regulation, and further examine therapeutic effects of antioxidants on skeletal muscle atrophy. Microarray data showed that the gene expression of many positive regulators for ROS production were up-regulated and the gene expression of many negative regulators for ROS production were down-regulated in mouse soleus muscle atrophied by denervation (sciatic nerve injury). The ROS level was significantly increased in denervated mouse soleus muscle or fasted C2C12 myotubes that had suffered from fasting (nutrient deprivation). These two muscle samples were then treated with N-acetyl-L-cysteine (NAC, a clinically used antioxidant) or pyrroloquinoline quinone (PQQ, a naturally occurring antioxidant), respectively. As compared to non-treatment, both NAC and PQQ treatment (1) reversed the increase in the ROS level in two muscle samples; (2) attenuated the reduction in the cross-sectional area (CSA) of denervated mouse muscle or in the diameter of fasted C2C12 myotube; (3) increased the myosin heavy chain (MHC) level and decreased the muscle atrophy F-box (MAFbx) and muscle-specific RING finger-1 (MuRF-1) levels in two muscle samples. Collectively, these results suggested that an increased ROS level was, at least partly, responsible for denervation- or fasting-induced skeletal muscle atrophy, and antioxidants might resist the atrophic effect via ROS-related mechanisms.

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“…MyomiRs, a class of miRNAs exclusively expressed or enriched in striated muscle, have been identified as essential determinants in regulatory networks of myogenesis, muscle fibre‐type composition, muscle growth, and homeostasis . Several miRNAs have also been shown to play a role in different experimental models of skeletal muscle atrophy, including miR‐18a, miR‐23a, miR‐27a, miR‐29b, miR‐351, miR‐422a, miR‐424(322)‐5p, miR‐542‐5p, and miR‐675 . AtromiRs have been dubbed as a collective term referring to miRNAs putatively involved in muscle atrophy, regulating processes and signalling pathways that contribute to muscle wasting .…”

Section: Introductionmentioning

confidence: 99%

Identification of microRNAs in skeletal muscle associated with lung cancer cachexia

Worp

Schols

Dingemans

et al. 2019

J cachexia sarcopenia muscle

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Background Cachexia, highly prevalent in patients with non-small cell lung cancer (NSCLC), impairs quality of life and is associated with reduced tolerance and responsiveness to cancer therapy and decreased survival. MicroRNAs (miRNAs) are small non-coding RNAs that play a central role in post-transcriptional gene regulation. Changes in intramuscular levels of miRNAs have been implicated in muscle wasting conditions. Here, we aimed to identify miRNAs that are differentially expressed in skeletal muscle of cachectic lung cancer patients to increase our understanding of cachexia and to allow us to probe their potential as therapeutic targets. Methods A total of 754 unique miRNAs were profiled and analysed in vastus lateralis muscle biopsies of newly diagnosed treatment-naïve NSCLC patients with cachexia (n = 8) and age-matched and sex-matched healthy controls (n = 8). miRNA expression analysis was performed using a TaqMan MicroRNA Array. In silico network analysis was performed on all significant differentially expressed miRNAs. Differential expression of the top-ranked miRNAs was confirmed using reverse transcriptionquantitative real-time PCR in an extended group (n = 48) consisting of NSCLC patients with (n = 15) and without cachexia (n = 11) and healthy controls (n = 22). Finally, these miRNAs were subjected to univariate and multivariate Cox proportional hazard analysis using overall survival and treatment-induced toxicity data obtained during the follow-up of this group of patients. Results We identified 28 significant differentially expressed miRNAs, of which five miRNAs were up-regulated and 23 were down-regulated. In silico miRNA-target prediction analysis showed 158 functional gene targets, and pathway analysis identified 22 pathways related to the degenerative or regenerative processes of muscle tissue. Subsequently, the expression of six topranked miRNAs was measured in muscle biopsies of the entire patient group. Five miRNAs were detectable with reverse transcription-quantitative real-time PCR analysis, and their altered expression (expressed as fold change, FC) was confirmed in muscle of cachectic NSCLC patients compared with healthy control subjects: miR-424-5p (FC = 4.5), miR-424-3p (FC = 12), miR-450a-5p (FC = 8.6), miR-144-5p (FC = 0.59), and miR-451a (FC = 0.57). In non-cachectic NSCLC patients, only miR-424-3p was significantly increased (FC = 5.6) compared with control. Although the statistical support was not sufficient to imply these miRNAs as individual predictors of overall survival or treatment-induced toxicity, when combined in multivariate analysis, miR-450-5p and miR-451a resulted in a significant stratification between short-term and long-term survival. Conclusions We identified differentially expressed miRNAs putatively involved in lung cancer cachexia. These findings call for further studies to investigate the causality of these miRNAs in muscle atrophy and the mechanisms underlying their differential expression in lung cancer cachexia.

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MicroRNA-351 inhibits denervation-induced muscle atrophy by targeting TRAF6

Cited by 26 publications

References 28 publications

Brucella Downregulates Tumor Necrosis Factor-α to Promote Intracellular Survival via Omp25 Regulation of Different MicroRNAs in Porcine and Murine Macrophages

Brucella Downregulates Tumor Necrosis Factor-α to Promote Intracellular Survival via Omp25 Regulation of Different MicroRNAs in Porcine and Murine Macrophages

Mechanistic Role of Reactive Oxygen Species and Therapeutic Potential of Antioxidants in Denervation- or Fasting-Induced Skeletal Muscle Atrophy

Identification of microRNAs in skeletal muscle associated with lung cancer cachexia

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