MicroRNAs 144, 145, and 214 are down-regulated in primary neurons responding to sciatic nerve transection

Zhang, Haiying; Zheng, Sujuan; Zhao, Jing; Zhao, Wei; Zheng, Linfeng; Zhao, Dan; Li, Jianming; Zhang, Xianfang; Chen, Zhibin; Yi, Xi-Nan

doi:10.1016/j.brainres.2011.01.067

Cited by 59 publications

(41 citation statements)

References 29 publications

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“…The values of PWMT and PWTL in the CCI group were significantly decreased, suggesting that the CCI model was successfully established in rats. Consistent with the results presented by Zhang et al (22), miR-145 expression levels in spinal cord tissue were significantly decreased in CCI rats. To further elucidate the role of miR-145 in CCI development, intrathecal injection of agomiR-145 was performed.…”

Section: Discussionsupporting

confidence: 92%

Role of miR-145 in chronic constriction injury in rats

Pang

Tang

Zhang

2016

Experimental and Therapeutic Medicine

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Abstract. The present study aims to investigate the effects and underlying mechanisms of miRNA-145 (miR-145) in rat models of chronic constriction injury (CCI). Rats were randomly divided into control, sham, CCI, agomiRNA (agomiR)-normal control (NC) and agomiR-145 groups (n=25 in each group); in addition, 30 rats with CCI were divided into small hairpin (sh)RNA-NC and shRNA-ras responsive element binding protein 1 (RREB1) groups. Paw withdrawal thermal latency (PWTL) and paw withdrawal mechanical threshold (PWMT) were detected. Reverse transcription-quantitative polymerase chain reaction was used to detect miR-145 expression levels, and western blotting was performed to measure RREB1 and phosphorylated-protein kinase B (p-AKT) expression levels. In addition, a dual luciferase reporter assay was conducted to identify the target gene of miR-145. PWMT and PWTL were decreased in CCI rats and this decrease was alleviated by miR-145 injection. At 1, 3, 5 and 7 days after CCI, miR-145 expression level in the spinal cord tissue of rats in the CCI group was significantly decreased compared with 1 day before CCI (P<0.05). Compared with the CCI group, miR-145 expression level in the agomiR-145 group was significantly higher (P<0.05). In addition, expression levels of RREB1 and p-AKT were significantly increased in the CCI group and significantly decreased in the agomiR-145 group (P<0.05). Furthermore, knockdown of RREB1 expression by shRNA-RREB1 significantly increased values of PWMT and PWTL, decreased expression levels of RREB1 and p-AKT, and increased miR-145 expression levels (P<0.05). Further investigation demonstrated that miR-145 can bind with RREB1 mRNA. In conclusion, miR-145 may be involved in the development of CCI through regulating the expression of RREB1.

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Section: Discussionsupporting

confidence: 92%

Role of miR-145 in chronic constriction injury in rats

Pang

Tang

Zhang

2016

Experimental and Therapeutic Medicine

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“…Several previous studies have shown that miR-34a can target SIRT1 in different tissues (Yamakuchi 2012). However, the expression of miR-34a does not seem to be altered in adult sensory neurons upon peripheral axotomy (Strickland et al 2011;Zhang et al 2011;Zhou et al 2011), suggesting that it is unlikely to target SIRT1, which is up-regulated drastically upon axotomy.…”

Section: Discussionmentioning

confidence: 89%

“…In mature animals, one study found that sensory axon regeneration in vivo was impaired in animals lacking the Dicer protein, which is crucial for microRNA processing , suggesting that microRNAs are potential novel regulators of axon regeneration. Indeed, several genetic profiling studies (Strickland et al 2011;Zhang et al 2011;Zhou et al 2011) have shown that the expression levels of many microRNAs are changed in adult mouse sensory neurons after the peripheral nerve injury, which leads to enhanced intrinsic axon growth capacity and robust axon regeneration. However, to date, no study has ever reported the roles of microRNAs in the regulation of mammalian axon regeneration in vivo.…”

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confidence: 99%

MicroRNA-138 and SIRT1 form a mutual negative feedback loop to regulate mammalian axon regeneration

et al. 2013

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Regulated gene expression determines the intrinsic ability of neurons to extend axons, and loss of such ability is the major reason for the failed axon regeneration in the mature mammalian CNS. MicroRNAs and histone modifications are key epigenetic regulators of gene expression, but their roles in mammalian axon regeneration are not well explored. Here we report microRNA-138 (miR-138) as a novel suppressor of axon regeneration and show that SIRT1, the NAD-dependent histone deacetylase, is the functional target of miR-138. Importantly, we provide the first evidence that miR-138 and SIRT1 regulate mammalian axon regeneration in vivo. Moreover, we found that SIRT1 also acts as a transcriptional repressor to suppress the expression of miR-138 in adult sensory neurons in response to peripheral nerve injury. Therefore, miR-138 and SIRT1 form a mutual negative feedback regulatory loop, which provides a novel mechanism for controlling intrinsic axon regeneration ability.

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“…Furthermore, changes (either increases or decreases) in miRNA expression have been found in many disease states (22)(23)(24). Bilateral sciatic nerve chronic constriction injury (bCCI) is commonly used as a model for studying human neuropathic pain, in which chromic gut sutures are used to ligate each sciatic nerve.…”

Section: Introductionmentioning

confidence: 99%

Differential expression of miRNAs in the nervous system of a rat model of bilateral sciatic nerve chronic constriction injury

Shen

et al. 2013

International Journal of Molecular Medicine

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Abstract. Chronic neuropathic pain is associated with global changes in gene expression in different areas of the nociceptive pathway. MicroRNAs (miRNAs) are small (~22 nt long) noncoding RNAs, which are able to regulate hundreds of different genes post-transcriptionally. The aim of this study was to determine the miRNA expression patterns in the different regions of the pain transmission pathway using a rat model of human neuropathic pain induced by bilateral sciatic nerve chronic constriction injury (bCCI). Using microarray analysis and quantitative reverse transcriptase-PCR, we observed a significant upregulation in miR-341 expression in the dorsal root ganglion (DRG), but not in the spinal dorsal horn (SDH), hippocampus or anterior cingulate cortex (ACC), in the rats with neuropathic pain compared to rats in the naïve and sham-operated groups. By contrast, the expression of miR-203, miR-181a-1 * and miR-541 * was significantly reduced in the SDH of rats with neuropathic pain. Our data indicate that miR-341 is upregulated in the DRG, whereas miR-203, miR-181a-1 * and miR-541 * are downregulated in the SDH under neuropathic pain conditions. Thus, the differential expression of miRNAs in the nervous system may play a role in the development of chronic pain. These observations may aid in the development of novel treatment methods for neuropathic pain, which may involve miRNA gene therapy in local regions. IntroductionNeuropathic pain is defined as pain arising as a direct consequence of a lesion or disease affecting either the peripheral or central nervous system (1,2). Although pain has been investigated in depth for decades, neuropathic pain is still frequently under-treated (3), due to poor understanding of its pathophysiological and molecular mechanisms. Several regions of the nociceptive pathway, including the anterior cingulate cortex (ACC), hippocampus, spinal dorsal horn (SDH) and dorsal root ganglion (DRG), are involved in the development and maintenance of neuropathic pain (4-9). Several recent studies have shown that peripheral and central sensitization are associated with global changes in gene expression in different regions of the pain transmission pathway, and that these changes may be part of the mechanisms behind neuropathic pain (10-13). In order to elucidate the molecular mechanisms underlying neuropathic pain, it is essential to determine how gene expression patterns are altered by nerve injuries and how these alterations lead to the development and maintenance of chronic pain.miRNAs are a large class of short non-coding RNAs (~22 nt long), many of which are expressed either predominantly or exclusively in the nervous system (14-21). Furthermore, changes (either increases or decreases) in miRNA expression have been found in many disease states (22-24). Bilateral sciatic nerve chronic constriction injury (bCCI) is commonly used as a model for studying human neuropathic pain, in which chromic gut sutures are used to ligate each sciatic nerve. This model is characterized by long-lasting cold all...

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MicroRNAs 144, 145, and 214 are down-regulated in primary neurons responding to sciatic nerve transection

Cited by 59 publications

References 29 publications

Role of miR-145 in chronic constriction injury in rats

Role of miR-145 in chronic constriction injury in rats

MicroRNA-138 and SIRT1 form a mutual negative feedback loop to regulate mammalian axon regeneration

Differential expression of miRNAs in the nervous system of a rat model of bilateral sciatic nerve chronic constriction injury

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