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13 publications mentioning rno-mir-365

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-365. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 293
Behavioral results suggested that overexpression of β-arrestin 2 abolished miR-365 mediated attenuation of morphine tolerance (Fig. 5F), Moreover, β-arrestin 2 expression remained upregulated after co-injection of β-arrestin 2 and miR-365 overexpression lentivirus vector (Fig. 5G). [score:10]
In conclusion, our results reveal that miR-365 is involved in morphine tolerance by regulating expression of β-arrestin 2. Overexpression of miR-365 results in decreased expression of the target gene β-arrestin 2 and attenuation of morphine tolerance. [score:10]
After chronic morphine infusion, miR-365 is downregulated, which alleviates translational repression of its target gene β-arrestin 2 and increases its expression. [score:10]
Downregulation of miR-365 is involved in development of morphine tolerance, and exogenous overexpression of miR-365 specifically alleviated morphine tolerance by targeting β-arrestin 2, a key component in MOR desensitization and endocytosis. [score:9]
After injection of the lentiviral vector- mediated miR-365, upregulated miR-365 was incorporated into an RNA -induced silencing complex (RISC) that mediated translational inhibition. [score:8]
After inducing lentiviral vector -mediated overexpression of miR-365, we found that overexpression of miR-365 specifically suppressed and reversed morphine tolerance. [score:7]
To identify target genes of miR-365 relevant to morphine tolerance, we searched for potential candidate targets using bioinformatics tools: TargetScan, miRanda, and miRDB. [score:7]
Recent studies found that miR-365 could inhibit vascular smooth muscle cell proliferation by down -regulating cyclin D1 and regulate Mycobacterium tuberculosis -induced active pulmonary tuberculosis via interleukin 6 expression 51 52. [score:7]
Immunofluorescent density of β-arrestin 2 (green) from the morphine treated group was downregulated (especially in the superficial lamina where CGRP is expressed) after injection of LV-miR-365. [score:6]
β-arrestin 2 is specifically downregulated in the spinal cord after overexpression of miR-365. [score:6]
In addition, it has been reported that miR-365 regulates expression of other target genes. [score:6]
After LV-miR-365 induction, spinal β-arrestin 2 protein expression and mRNA levels were both down-regulated in a time -dependent manner. [score:6]
As MOR are most abundant in the superficial lamina, the data indicate that downregulation of β-arrestin 2 may influence MOR function after miR-365 overexpression. [score:6]
Because the target genes of let-7 (MOR) and miR-23b (MOR1) interact with the target gene of miR-365 (β-arrestin 2), we cannot rule out that there may be a relationship between these miRNAs and miR-365. [score:5]
Taken together, these findings suggest that miR-365 overexpression attenuates morphine tolerance at least partly by decreasing β-arrestin 2 expression. [score:5]
In addition, among the target genes of miR-365, some target genes participate in morphine tolerance (described in the discussion). [score:5]
Moreover, in rats with morphine infusion, the increased spinal β-arrestin 2 expression was reversed by overexpression of miR-365 but not by the LV-control treatment (Fig. 5C). [score:5]
However, we observed that lentiviral vector -mediated overexpression of miR-365 did not fully restore the analgesic effect of morphine, although the expression of miR-365 was robustly increased. [score:5]
miR-365 expression was not altered on day 3 after morphine injection, however, on day 5 it began to decline (Fig. 1D), and these changes were consistent with development of morphine tolerance. [score:4]
To our knowledge, this is the first demonstration of a regulatory role for miR-365 in the development of morphine tolerance through regulation of β-arrestin 2. We showed that miR-365 plays a vital role in morphine tolerance, ranging from molecular changes in cells to behavioral changes in animals. [score:4]
miR-365 directly targets β-arrestin 2. β-arrestin 2 is responsible for miR-365 -mediated morphine tolerance. [score:4]
miR-365 is down-regulated in the spinal cord of morphine-tolerant rats. [score:4]
These findings suggest that miR-365 directly targets the β-arrestin 2 3′-UTR in a sequence-specific manner. [score:4]
A previous study found that miR-365 was upregulated after long-term morphine treatment in the mouse hippocampus and primary cultures of rat hippocampal neurons 37. [score:4]
Studies reported that miR-365 is upregulated in human breast cancer 34, and involved in carcinogenesis of small lung cancer and colon cancer 35 36. [score:4]
At day 5 and day 7 after morphine injection, β-arrestin 2 was gradually increased (Fig. 5A) and inversely correlated with miR-365 downregulation (Fig. 1E), suggesting that miR-365 and β-arrestin 2 are inversely correlated. [score:4]
miR-365 directly targets the β-arrestin 2 3′-UTR. [score:4]
Downregulation of miR-365 in the spinal cord after induction of morphine tolerance. [score:4]
Therefore, miR-365 targeting of β-arrestin 2 is a suitable and promising approach for treatment of morphine tolerance. [score:3]
Left panel: Chronic morphine infusion sets up a cascade of events that lead to decreased levels of miR-365 and increased expression of β-arrestin 2, which ultimately causes morphine tolerance. [score:3]
The current study is the first to demonstrate that miR-365 prevents and reverses development and maintenance of morphine tolerance through regulation of GPCR binding protein β-arrestin 2. However, this study has several limitations. [score:3]
miR-365 expression was gradually increased above basal levels 5 days after intrathecal LV-miR-365 injection and remained increased 10 days after treatment with LV-miR-365 (Fig. 3B). [score:3]
The 3′-UTR sequence (including the predicted mir-365 target sequence) of β-arrestin 2 was cloned into a reporter vector downstream of the Renilla luciferase gene. [score:3]
However, neither lentiviral -mediated overexpression of miR-365 nor a miR-365 mimic can satisfy these requirements. [score:3]
However, our in situ hybridization data showed that miR-365 was located in neurons of spinal cord, so we focused on β-arrestin 2 as a target of miR-365. [score:3]
In addition, the mRNA level of β-arrestin 2 was also decreased in the miR-365 overexpression group (Fig. 5D). [score:3]
The data showed that miR-365 was expressed in the dorsal horn of the spinal cord. [score:3]
The decreased level of β-arrestin 2 mRNA may be attributed to overexpression of miR-365, which cleaved the 3′-UTR of β-arrestin 2 after partially binding to it. [score:3]
Co-immunostaining revealed high expression of miR-365 in the neuron specific NeuN -positive neurons of the spinal dorsal horn (Fig. 2). [score:3]
The mutated vector (pYr-Arrb2-3U-Del) was constructed by a partial deletion of the miR-365 targeting sequence (5′-GAGAGGTAGGGGTGGGCAGGACTGAGGTCCACTGCCCTTGCGGGTAGGAGGGTCCCAGCCTCTCCTCCTTCCCCGTTCGTCCACCCGAGATACACACTGGACCCATCACTCGTTGAAAGTgtaATCTTTTGACTTCAGCTCTGCCACCCCAGCCCTGCTCCCTAGGGTGGCAAGCTGTGTACACACCTAAAGTTTTGGGAAGGGAAGGGAACACTGAAAGCAAGGAGTGAATGTAGAGAAAAGGAGTAGAA-3′). [score:3]
To explore further the localization and expression of miR-365 in the spinal cord, miRNA-specific in situ hybridization and staining were employed. [score:3]
Lentivirus -mediated overexpression of miR-365 prevents and reverses morphine tolerance in rats. [score:3]
Our luciferase assay results suggest that miR-365 regulates β-arrestin 2 expression levels. [score:3]
In our study, β-arrestin 2 was identified as a target gene of miR-365. [score:3]
Therefore, we examined whether β-arrestin 2 is a direct target of miR-365 using a luciferase assay. [score:3]
miR-365 was one of the most robustly reduced of these miRNAs, and the expression levels of miR-365 were confirmed by qPCR (Fig. 1C). [score:3]
The data from staining showed that miR-365 was expressed in the superficial lamina of the spinal cord dorsal horn where MORs are most abundant. [score:3]
How to cite this article: Wang, J. et al. miR-365 targets β-arrestin 2 to reverse morphine tolerance in rats. [score:3]
Overexpressing miR-365 using lentivirus-miR-365 might provide a promising and novel approach to treatment of morphine tolerance. [score:3]
In rats with saline injection, the data showed that β-arrestin 2 expression levels gradually decreased after injection of LV-miR-365 (Fig. 5B). [score:3]
Lentiviral -mediated overexpression of miR-365 prevents and reverses morphine tolerance in rats. [score:3]
We cannot exclude the possibility that other target genes of miR-365 are involved in miR-365 -induced attenuation of morphine tolerance. [score:3]
To explore the functional relevance between miR-365 and β-arrestin 2, we further examined if miR-365 affects β-arrestin 2 expression levels in vivo. [score:3]
Moreover, miR-365 also plays a role in the CNS, in which miR-365 is overexpressed in the rat hippocampus after status epilepticus induced by amygdala stimulation 29. [score:3]
We found that overexpression of miR-365 significantly reversed morphine tolerance (Fig. 3D). [score:3]
We initially considered interleukin -6 and β-arrestin 2 as target genes of miR-365. [score:2]
Furthermore, Fig. 4B shows that the miR-365 binding site is well conserved among mammals, which indicates that β-arrestin 2 regulation by miR-365 is functionally important. [score:2]
Maybe this is because miR-365 only exerts its regulatory effects at the post-transcription level and is not involved in gene transcription. [score:2]
Compared with the normal saline group, miR-365 expression was decreased on day 7 after morphine administration (Fig. 1E). [score:2]
In our present study, miR-365 was identified as a key functional miRNA for regulation of morphine antinociceptive tolerance. [score:2]
Schematic diagram for the proposed mechanism of morphine tolerance regulation by miR-365. [score:2]
Previous studies have reported that multiple miRNA -based pathways, such as let-7 and miR-23b, contributed to morphine tolerance 10 27, and some of these show the same deregulation pattern of miR-365. [score:2]
The data of our study showed a new role of miR-365 in regulating morphine tolerance. [score:2]
We found that miR-365 had no effect on luciferase activity (Fig. 4A). [score:1]
The pYr-Arrb2-3U vector and pYr-Arrb2-3U-Del vector constructs with or without either the miR-365 mimic (50 nM) or the scrambled control (50 nM) were transfected into HEK293 cells (70% confluence) (Lipofectamine 2000, Invitrogen). [score:1]
Pri-miR-365 and negative control sequences were cloned into the pGCsil-GFP vector (GENECHEM) to generate the lentivirus -mediated miR-365 vector (LV-miR-365) and the lentivirus negative control vector (LV-control). [score:1]
However, none of these miRNAs is from the same gene family as miR-365. [score:1]
After cotransfection of HEK293 cells with the reporter vector containing miR-365, luciferase activity with the β-arrestin 2 3′-UTR was attenuated (Fig. 4A). [score:1]
Cell-specific localization of miR-365 in the spinal cord as assessed by in situ hybridization with subsequent coimmunofluorescence staining of the spinal cord for miR-365 (red), neurons using NeuN antibody (green), astrocytes using GFAP antibody (green), and microglia using Iba1 antibody (green). [score:1]
LV-control vector or LV-miR-365 vector was administered on day 7 after establishment of morphine tolerance. [score:1]
The seed sequence is indicated by bold letters, while the pairing sequence of miR-365 is in red bold letters. [score:1]
These results suggest that miR-365 in the spinal cord contributes to modulation of morphine tolerance. [score:1]
LV-β-arrestin 2 or LV-scramble was co -injected with LV-miR-365 3 days before chronic morphine injection. [score:1]
In situ hybridization and immunochemistryA digoxin-labeled locked nucleic acid (LNA) detection probe for miR-365 was purchased from Exiqon. [score:1]
Right panel: After a host cell is infected with a lentivirus, the viral genome is integrated into the host genome in the nucleus to yield primary-miR-365. [score:1]
Briefly, the 3′-UTR of β-arrestin 2 (5′-GAGAGGTAGGGGTGGGCAGGACTGAGGTCCACTGCCCTTGCGGGTAGGAGGGTCCCAGCCTCTCCTCCTTCCCCGTTCGTCCACCCGAGATACACACTGGACCCAtcactcgttgaaagtgggcattaATCTTTTGACTTCAGCTCTGCCACCCCAGCCCTGCTCCCTAGGGTGGCAAGCTGTGTACACACCTAAAGTTTTGGGAAGGGAAGGGAACACTGAAAGCAAGGAGTGAATGTAGAGAAAAGGAGTAGAA-3′) was generated by gene synthesis, which contained the seed sequence complementary to miR-365 (5′-GGGCATT-3′), was subcloned downstream of the Renilla luciferase reporter gene into the psiCHECK-2 vector (Promega). [score:1]
To further explore the role of β-arrestin 2 in miR-365 mediated attenuation of morphine tolerance, rats were simultaneously injected intrathecally with LV-β-arrestin 2 and LV-miR-365 before chronic morphine infusion. [score:1]
To confirm delivery of lentivirus (LV)-miR-365 or LV-control into neuronal cells of the spinal cord, transfected cells in the spinal cord were visualized by GFP fluorescence. [score:1]
However, miR-365 has not been linked to morphine tolerance in the study. [score:1]
For this reason, miR-365 was studied further to determine its role in morphine tolerance. [score:1]
Rats were injected with control or miR-365 lentivirus vector 3 days before chronic normal saline infusion. [score:1]
To explore the role of miR-365 in modulation of morphine tolerance at the behavioral level, we first pretreated rats with intrathecal injection of LV-miR-365, LV-control vector, or vehicle (normal saline) 3 days before chronic morphine or normal saline infusion. [score:1]
After pretreatment with pepsin, sections were prehybridized in hybridization buffer for 4 h at 47 °C followed by hybridization with denaturation hybridization buffer containing 2 pmol/L miR-365 or a negative control (scrambled probe) at 48 °C overnight. [score:1]
Cell-specific localization of miR-365 in the spinal cord. [score:1]
Primary-miR-365 is processed to yield premature-miR-365, which is exported to the cytoplasm where mature miR-365 is generated and incorporated into the RISCs that are programmed by microRNA. [score:1]
To identify further the miR-365 binding sequence within the 3′-UTR, we mutated the predicted seed sequence with a partial deletion (Fig. 4B). [score:1]
A digoxin-labeled locked nucleic acid (LNA) detection probe for miR-365 was purchased from Exiqon. [score:1]
Then we post -treated rats with LV-control or LV-miR-365 vector on day 7 after establishment of morphine tolerance. [score:1]
β-arrestin 2 mRNA was then recruited to the RISC, binding to miR-365 with its 3′-UTR. [score:1]
Further studies will be required to explore the specific interaction of these miRNAs and miR-365. [score:1]
Further insight into the role of miR-365 in neurons will enhance our understanding of the molecular mechanisms of morphine tolerance. [score:1]
Further studies are required to clarify the distinct role, therapeutic impacts, and potential side effects of miR-365 modulation of morphine tolerance in humans. [score:1]
The next day, slides were rinsed 3 times and incubated with Alexa Fluor 488-conjugated secondary antibodies (1:800, Jackson) for 2 h. For detecting LV-miR-365 and β-arrestin 2, we incubated the slides with rabbit anti-GFP (1:200 Abcam), rabbit anti-β-arrestin 2 (1:200 Abcam), mouse anti-NeuN, and mouse anti-CGRP (1:200 Abcam). [score:1]
After intrathecal administration of LV-miR-365 or LV-control, we found that many neuronal cell bodies were highly fluorescent, suggesting that the lentivirus was successfully transfected into neuronal cells (Fig. 3A). [score:1]
The pGCsil-miR-365-GFP vector (20 μg) with pHelper 1.0 Vector (packaging plasmid, 15 μg) and pHelper 2.0 vector (envelop plasmid, 10 μg) were cotransfected into HEK293T cells using Lipofectamine 2000 (Invitrogen). [score:1]
Rats treated with saline infusion (Vehicle + NS, LV-control + NS and LV-miR-365 + NS) showed no significant difference in %MPE during the 7 days. [score:1]
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2.4. miR-365 Directly Targets HDAC4 Leading to Down-Regulation of HDAC4 Expression. [score:9]
We examined the mRNA level of hypertrophic marker gene Col X. Indeed, overexpression of miR-365 significantly up-regulated Col X and further increase of IL-1β induced the up-regulation of Col X (Figure 2C). [score:9]
The up-regulation of miR-365 further contributes to cartilage catabolic effects in OA through inhibition of its target HDAC4. [score:8]
Although the critical role of miR-365 in cartilage maintenance may be explained largely by identifying HDAC4 as its direct target, miRNAs are believed to regulate multiple target mRNAs. [score:7]
Understanding the regulation of miR-365 in this pathophysiological condition is of great importance and could open up new therapeutic avenues targeting the disease. [score:6]
miR-365 overexpression and IL-1β treatment have a synergistic effect on the down-regulation of HDAC4 (Figure 6B). [score:6]
To investigate whether the expression of miR-365 was induced by IL-1β, primary human chondrocytes were stimulated with IL-1β for 24 h. IL-1β stimulation of chondrocytes resulted in significant up-regulation of miR-365 expression (Figure 2A). [score:6]
More interestingly, IL-1β significantly reduced expression of HDAC4 mRNA, which resembled the effect of miR-365 overexpressing chondrocytes (Figure 6B). [score:5]
Primary cultured human chondrocytes were serum starved overnight and then treated with 10 ng/mL recombinant human IL-1β (Roche, Branchburg, NJ, USA) for 24 h. Human miR-365 mimic, miR-365 inhibitor and their negative control mimics or inhibitors were obtained from Dharmacon (Thermofisher Scientific). [score:5]
Western blotting results further confirmed the inhibition of HDAC4 mRNA and protein expression by miR-365 while anti–miR-365 enhanced the mRNA and protein level of HDAC4 in human chondrocytes (Figure 5B,C). [score:5]
The expression of miR-365 was significantly up-regulated by cyclic loading compared with its non-load control (Figure 1A). [score:5]
Xu Z. Xiao S. B. Xu P. Xie Q. Cao L. Wang D. Luo R. Zhong Y. Chen H. C. Fang L. R. miR-365, a novel negative regulator of interleukin-6 gene expression, is cooperatively regulated by Sp1 and NF-κB J. Biol. [score:5]
Inhibition of miR-365 or Overexpression of HDAC4 Impairs IL-1β Induction of MMP13 mRNA. [score:5]
Manipulation of the expression of miR-365 in articular chondrocytes by a miR-365 inhibitor may be a potent therapeutic for the prevention and treatment of OA. [score:5]
The expression of miR-365 was significantly up-regulated in OA cartilage compared with normal cartilage (Figure 3D). [score:5]
To further clarify the molecular mechanism underlying miR-365 on OA pathogenesis, we are interested in identifying the direct target of miR-365 that may be involved in OA development. [score:5]
Furthermore, inhibition of miR-365 reduced the IL-1β induced catabolic effect as shown by significant inhibition of MMP13 (Figure 6C). [score:5]
2.2. miR-365 is Up-Regulated by Pro-inflammatory Cytokine IL-1β and is Essential for Cartilage Degeneration. [score:4]
To further determine whether miR-365 is up-regulated in OA cartilage in vivo, we used the surgical arthritis mo del to experimentally induce OA pathogenesis, in which the articular cartilage was exposed to an excessive mechanical load, due to joint instability caused by surgical resection of the anterior cruciate ligament (ACL) in rats. [score:4]
We further show HDAC4 is a direct target of miR-365, which mediates mechanical stress and inflammation in OA pathogenesis, thereby leading to accelerated cartilage destruction. [score:4]
This is consistent with our study that cyclic loading and IL-1 both up-regulate the transcription of miR-365 through activation of NF-κB. [score:4]
To identify whether HDAC4 is a direct target of miR-365 in human chondrocytes, we transfected a wild-type HDAC4 3′-UTR construct containing a putative miR-365 binding sequence. [score:4]
HDAC4 protein expression is modulated by miR-365, and this regulatory effect is driven by the miR-365 conserved seed sites within the 3′-UTR of HDAC4. [score:4]
In this study, we showed that HDAC4 is a direct target of miR-365 in human articular chondrocytes at different levels. [score:4]
Furthermore, we found that the construct bearing mutations at a putative miR-365 binding site completely abolished the inhibitory effect of miR-365 (Figure 5A). [score:4]
We therefore asked whether miR-365 is sufficient to up-regulate metallopeptidase 13 (MMP13), a crucial effector of OA cartilage destruction. [score:4]
Therefore, cyclic loading transcriptionally up-regulates miR-365 through NF-κB signaling. [score:4]
In vivo work using transgenic animal mo dels to overexpress miR-365 or knockout miR-365 in cartilage will be needed to establish the definite etiologic answer for miR-365 in OA pathogenesis. [score:4]
We have identified that mechanical loading up-regulated miR-365 in growth plate chondrocytes. [score:4]
MMP13 was significantly up-regulated by transfection of chondrocytes with miR-365 mimic and was exacerbated by IL-1β treatment (Figure 2D). [score:4]
A Luciferase reporter assay revealed that overexpression of miR-365 significantly inhibited reporter activity in human chondrocytes. [score:4]
Furthermore, miR-365 is transcriptionally up-regulated by cyclic loading and IL-1β stimulation through the activation of NF-κB signaling in the articular chondrocytes. [score:4]
This further supports the notion that HDAC4 may be a direct target of miR365, which mediates OA pathogenesis. [score:4]
Taken together, these findings suggest that miR-365 directly targets HDAC4 in human chondrocytes and mediates its catabolic effects. [score:4]
Cyclic Loading Transcriptionally Up-Regulates miR-365 through NF-кB Signaling. [score:4]
To further confirm that miR-365 contributes to OA pathogenesis through HDAC4, we examined the expression of HDAC4 in human OA cartilage. [score:3]
Therefore, miR-365 contributes to OA pathogenesis by targeting HDAC4 through two mechanisms: hypertrophic conversion of articular chondrocytes through RUNX2 and MEF2C (Figure 5C) and promoting inflammatory cytokine production to increase catabolic effects. [score:3]
We found that cyclic loading in 3D chondrocytes and disruption of extracellular matrix (ECM) by mechanical instability induced by anterior cruciate ligament transection (ACLT) surgery, triggered increased miR-365 expression in cartilage. [score:3]
To further confirm relations between OA and miR-365 in human cartilage, we quantify the miR-365 expression level in primary OA (PA) and traumatic OA (TA) groups, which were divided according to the patient’s medical history. [score:3]
In conclusion, our results collectively indicate that miR-365 acts as a mechanically induced mediator of osteoarthritic cartilage destruction, by directly regulating HDAC4. [score:3]
We have found a significant difference in miR-365 expression in the OA vs. [score:3]
The miR-365 expression levels in the lesion area were significantly higher than the corresponding non-lesion control area in both the primary OA and traumatic OA groups (Figure 4A,B). [score:3]
We have shown that miR-365 is expressed at a higher level in OA cartilage (Figure 4B,C). [score:3]
2.3. miR-365 Expression Is Increased in Osteoarthritis (OA) Cartilage. [score:3]
In this study, we observed mechanical responsive miR-365 is expressed at higher levels in both primary OA and traumatic OA cartilage. [score:3]
Overexpression of miR-365 induces chondrocyte differentiation marker Ihh and MMP13 and exacerbates the IL-1 induced catabolic effects in chondrocytes. [score:3]
miR-365 is expressed at higher levels in human OA cartilage from primary OA patients as well as OA patients with traumatic history, supporting its pathological significance. [score:3]
Total protein was extracted from human articular chondrocytes 48 h post-transfection of miR-365 mimic or inhibitor and their controls. [score:3]
The expression of miR-365 in OA chondrocytes was significantly higher than that in the relative normal chondrocytes (Figure 3A). [score:3]
In this study, we explain a possible causal relationship between the mechanical stress and pro-inflammatory stimuli responsive miR-365, which regulates catabolic effects in human articular chondrocytes and mediates OA development. [score:3]
It remains unknown whether this involves regulation of miR-365 or other mechanical sensitive miRNAs. [score:2]
Therefore, the role of miR-365 in cartilage homeostasis may involve the regulation of additional genes. [score:2]
pGL-HDAC4-mut was derived from pGL-HDAC4 by mutating 3 bases pairs within miR-365 seed sites within the HDAC4 3′-UTR sequence using the QuikChange XL Site-directed Mutagenesis kit (Stratagene, La Jolla, CA, USA). [score:2]
Cyclic loading is sufficient for the transcriptional regulation of miR-365 through NF-κB signaling. [score:2]
As a result, the downstream Runx2 and MEF2C were regulated by miR-365 and contribute to hypertrophic conversion of chondrocytes in OA cartilage. [score:2]
To determine whether miR-365 is involved in OA pathogenesis, we compared its expression level between normal and OA chondrocytes. [score:2]
However, we failed to conclude that traumatic OA cartilage expresses higher levels of miR-365 compared with primary OA cartilage. [score:2]
miR-365 expression level was quantified with the Taqman microRNA assays specific for mature miR-365 (Life Technologies). [score:2]
Furthermore, in the late stage of OA, stress from the combination of overload and inflammatory cytokines further increases miR-365, leading to cartilage degradation. [score:1]
However, our data demonstrate miR-365 is induced by mechanical stress as well as an inflammatory cytokine which contributes to the pathological sequence of OA progression. [score:1]
We aim to address the role of mechanical sensitive miR-365 in OA by using human articular chondrocytes, an animal mo del and osteoarthritis patients and traumatic osteoarthritis patients. [score:1]
Here, we identify that miR-365 is a mechanically induced mediator of cartilage degeneration. [score:1]
The luciferase reporter plasmid TSS-1348, TSS-1097, TSS-705, and TSS-336, which contains the 1348-, 1097-, 705-, and 336-bp proximal promoter sequences upstream of TSS of miR-365, respectively, were a generous gift from Professor Liu-Rong Fang from Hua-Zhong agriculture University, Wuhan, China [24]. [score:1]
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Other miRNAs from this paper: rno-mir-338
Compared with the morphine tolerance group, the GFAP protein expression in the miR-365 mimic group decreased (P < 0.05), while the GFAP protein expression in the miR-365 inhibitor group increased (P < 0.05); the GFAP protein expression in the miR-365 NC group showed no significant change (P > 0.05), as shown in Fig.   6. This led to the suggestion that miR-365 overexpression might lower GFAP protein expression, inhibiting the activation of astrocyte. [score:14]
The results obtained showed that when compared with the morphine tolerance group, there was an increase in miR-365 expression and a decrease in the β-arrestin2, ERK, CREB protein expressions, contents of IL-1β, TNF-α, IL-18 and GFAP expression in the miR-365 mimic group, while the miR-365 inhibitor group displayed an opposite trend. [score:8]
The miR-365 expression in the miR-365 inhibitor group decreased, while the mRNA expressions of β-arrestin2, ERK and CREB increased (all P < 0.05). [score:7]
Previous data showed that miR-365 was robustly decreased in the spinal cord after chronic morphine administration, during which, the overexpression of miR-365 prevents and reverses morphine tolerance, and increased expression of miR-365 will result in a decreased expression of β-arrestin 2 protein [4]. [score:7]
The miR-365 expressions in the miR-365 NC group, β-arrestin2, ERK and CREB mRNA showed no significant difference (P > 0.05), as shown in Fig.   3. It can be concluded that miR-365 overexpression might reduce the mRNA expressions of β-arrestin2, ERK and CREB. [score:7]
Compared with the morphine tolerance and miR-365 NC groups, the protein expressions of β-arrestin2, p-ERK and p-CREB in the miR-365 mimic group decreased (P < 0.05), while the protein expressions of β-arrestin2, p-ERK and p-CREB in the miR-365 inhibitor group increased (P < 0.05) (Fig.   4). [score:6]
The collective results showed strong evidence that miR-365 could relieve the development of morphine analgesic tolerance to some degree by targeting β-arrestin2 through reducing the content of IL-1β, TNF-α and IL-18 and inhibiting the activation of astrocyte and the ERK/CREB signaling pathway. [score:6]
The pretreatment with ERK inhibitor notably suppressed miR-365 promoter activity, which indicated the regulatory role of ERK on the miR-365 transcription [28]. [score:6]
As reflected in previous study, the up-regulated expression of miR-365 could reverse the established morphine tolerance [4]. [score:6]
Our study also shows that compared with rats in the morphine tolerance group, the β-arrestin2, ERK and GFAP mRNA expressions were reduced in the miR-365 mimic group in a time -dependent manner, indicating that the overexpression of miR-365 might attribute to decreased β-arrestin2 mRNA expressions [4]. [score:6]
Compared with the control group, the miR-365 expression in the morphine tolerance, miR-365 mimic, miR-365 inhibitor and miR-365 NC groups decreased, while the mRNA expressions of β-arrestin2, ERK, and CREB increased (all P < 0.05). [score:6]
Overexpressed miR-365 inhibits the activation of ERK/CREB signaling pathway. [score:5]
The cells were independently transfected with pMIR-REPORT-arr-3 U and miR-365 NC, pMIR-REPORT-arr-3 U and miR-365 mimics, pMIR-REPORT-arr-3 U and miR365 inhibitors, pMIR-REPORT-arr-3 U-Del and miR365 mimics, pMIR-REPORT-arr-3 U-Del and miR-365 inhibitors, and pMIR-REPORT-arr-3 U-Del and miR365 NC. [score:5]
The activity of luciferase did not change notably in HEK293 cells that were transfected with pMIR-REPORT-arr-3 U-Del and miR-365 mimics, pMIR-REPORT-arr-3 U-Del and miR-365 inhibitors, and pMIR-REPORT-arr-3 U-Del and miR-365 NC, as shown in Fig. 2-B. It can be concluded that β-arrestin2 might be a target gene of miR-365. [score:5]
In conclusion, the results obtained during this study demonstrated that miR-365 could reduce the susceptibility to morphine analgesic tolerance by targeting β-arrestin2, resulting in the reduction of the contents of IL-1β, TNF-α and IL-18 and inhibiting the activation of astrocyte and the ERK/CREB signaling pathway. [score:5]
We can conclude that miR-365 overexpression might reduce the protein expressions of β-arrestin2, ERK and CREB, thus inactivating the ERK/CREB signaling pathway. [score:5]
The overexpression of miR-365 decreases the mRNA expressions of β-arrestin2, ERK and CREB. [score:5]
In the miR-365 inhibitor group, the rats were injected with 10 μL morphine in the morning and afternoon every day for seven days as well as being administered with 10 μL of miR-365 inhibitors (5’-AUAAGGAUUUUUAGGGGCAUUA-3′) before morphine administration in the morning. [score:5]
They were randomly divided into the control (injected with saline), morphine tolerance, miR-365 mimic + morphine (miR-365 mimic), miR-365 inhibitor + morphine (miR-365 inhibitor) and miR-365 negative control (NC) + morphine (miR-365 NC) groups, each group containing 8 rats. [score:5]
Forty male SD rats were selected and randomly divided into 5 groups: the control group, morphine tolerance group, miR-365 mimic + morphine (miR-365 mimic) group, miR-365 inhibitor + morphine (miR-365 inhibitor) group and miR-365 negative control (NC) + morphine (miR-365 NC) group. [score:5]
The results of this experiment suggest that by targeting β-arrestin2 to reduce the contents of IL-1β, TNF-α and IL-18 and by inhibiting the activation of ERK/CREB signaling pathway, miR-365 could lower morphine analgesic tolerance. [score:5]
Compared with the control group, the GFAP protein expression of rats in the morphine tolerance, miR-365 mimic, miR-365 inhibitor and miR-365 NC groups all increased (P < 0.05). [score:4]
Compared with the morphine tolerance group, the miR-365 expression in the miR-365 mimic group increased, while the mRNA expressions of β-arrestin2, ERK and CREB decreased (all P < 0.05). [score:4]
Compared with the control group, the protein expressions of β-arrestin2, p-ERK and p-CREB in the morphine tolerance, miR-365 mimic, miR-365 inhibitor and miR-365 NC groups increased (P < 0.05). [score:4]
Fig. 3Expressions of miR-365, β-arrestin2, ERK and CREB mRNA of rats in spinal cord tissues in each group after administration at day 7. Note: N = 8; [*], P < 0.05 compared with the control group; [#], P < 0.05 compared with the morphine tolerance group; ERK, extracellular signal-regulated kinase; CREB, cAMP-response element binding protein; NC, negative control was used to detect the protein expressions of β-arrestin2, ERK and CREB. [score:4]
Fig. 3Expressions of miR-365, β-arrestin2, ERK and CREB mRNA of rats in spinal cord tissues in each group after administration at day 7. Note: N = 8; [*], P < 0.05 compared with the control group; [#], P < 0.05 compared with the morphine tolerance group; ERK, extracellular signal-regulated kinase; CREB, cAMP-response element binding protein; NC, negative control Western blotting was used to detect the protein expressions of β-arrestin2, ERK and CREB. [score:4]
2009.10.010 20004063 4. Wang J, Xu W, Zhong T, Song Z, Zou Y, Ding Z, et al. miR-365 targets beta-arrestin 2 to reverse morphine tolerance in rats. [score:3]
However, neither the lentiviral -mediated overexpression of miR-365 nor a miR-365 mimic met these requirements. [score:3]
The %MPE in the miR-365 NC group was much stronger than that of the morphine tolerance in the miR-365 NC groups (P < 0.05), while the %MPE in the miR-365 inhibitor group was weaker than the morphine tolerance in the miR-365 NC groups (P < 0.05). [score:3]
Lentiviral packaging products, including miR-365 mimics, miR-365 inhibitors and miR-365 NC were purchased from Shanghai Genechem Co. [score:3]
The pMIR-REPORT-arr-3 U (GGGCATT was the binding sites of miR-365 in sequence) and pMIR-REPORT-arr-3 U-Del (GT was the mutant site of GGGCATT), restriction sites of Xhol I and Not I were put into the 5’end and 3’end of target fragments respectively, and were then converted into DH5α, and the plasmids were extracted for sequencing (Shanghai Invitrogen Biotechnology Corporation, Shanghai, China). [score:3]
Note: A, binding sites for miR-365 and 3’ UTR of β-arrestin2; B, dual luciferase reporter gene assay for miR-365 and 3’ UTR of β-arrestin2; N = 3; [*], P < 0.05 compared with the co -transfected group of pMIR-REPORT-arr-3 U and miR-365 NC; NC, negative control RT-qPCR was used to detect miR-365 expression and the mRNA expressions of β-arrestin2, ERK and CREB. [score:3]
Overexpressed miR-365 represses the activation of astrocyte. [score:3]
The above results implied that miR-365 overexpression might decline the contents of IL-1β, TNF-α and IL-18. [score:3]
As an onco-miR, miR-365 is highly expressed in both cells and clinical specimens of malignancies [6], and proved to be involved in cell differentiation, proliferation and apoptosis of cells including lung cancer cells and endothelial cells [7, 8]. [score:3]
β-arrestin2 is a target gene of miR-365. [score:3]
Overexpressed miR-365 decreases contents of IL-1β, TNF-α and IL-18. [score:3]
The above findings indicated that miR365 overexpression might increase the %MPE. [score:3]
β-arrestin2 was the target gene of miR-365. [score:3]
The analgesic effect of the miR-365 mimic group and the miR-365 inhibitor group also decreased gradually over time (Fig.   1). [score:3]
Compared with the control group, the contents of IL-1β, TNF-α and IL-18 in the morphine tolerance, miR-365 mimic, miR-365 inhibitor and miR-365 NC groups markedly increased (all P < 0.05). [score:2]
Compared with the morphine tolerance group, the protein expressions of β-arrestin2, p-ERK and p-CREB showed no significant changes in the miR-365 NC group (P > 0.05). [score:2]
Compared with the morphine tolerance group, the contents of IL-1β, TNF-α and IL-18 in the miR-365 NC group showed no significant differences (P > 0.05); the contents of IL-1β, TNF-α and IL-18 in the miR-365 mimic group decreased (P < 0.05), while the content of IL-1β, TNF-α and IL-18 in the miR-365 inhibitor group increased (P < 0.05) (Fig.   5). [score:2]
A dual luciferase reporter gene assay was performed to confirm the relationship between miR-365 and β-arrestin2, RT-qPCR was used to detect miR-365, β-arrestin2, ERK and CREB mRNA expressions, western blotting was used to evaluate the protein expressions of β-arrestin2, ERK, p-ERK, CREB and p-CREB, ELISA was used to detect the contents of IL-1β, TNF-α and IL-18, while immunofluorescence staining was used to measure the GFAP expression. [score:2]
The results of bioinformatics showed the matching sequence of miR-365 and 3’ UTR in β-arrestin2, as shown in Fig.   2-A. The activity of luciferase in HEK293 cells that were transfected with pMIR-REPORT-arr-3 U and miR-365 mimics decreased significantly compared to those co -transfected with pMIR-REPORT-arr-3 U and miR-365 NC (P < 0.05), while the activity of luciferase in HEK293 cells transfected with pMIR-REPORT-arr-3 U and miR-365 inhibitors increased significantly (P < 0.05). [score:2]
The findings showed that compared with the rats in the morphine tolerance group, higher miR-365 expression and %MPE were found in the miR-365 mimic group, suggesting that miR-365 and %MPE may be related to morphine administration. [score:2]
Fig. 2Dual luciferase reporter gene assay illustrating that miR-365 targeted β-arrestin2. [score:2]
Compared with the morphine tolerance and miR-365 NC groups, the %MPE showed significant difference in the miR-365 mimic and miR-365 inhibitor groups. [score:2]
According to the directions of the miR-365 detection kit (LK-0101A, Shanghai Novland BioPharma, Shanghai, China), reaction conditions comprised of 3 min at 94 °C, 1 cycle, 20 s at 94 °C and 40 s at 62 °C, 40 cycles. [score:2]
Therefore, the following study was conducted to explore the effects of miR-365 on morphine analgesic tolerance by regulating β-arrestin2 in a rat mo del. [score:2]
The morphine tolerance in the miR-365 NC group began to appear 3 days after administration, and apparent tolerance was observed 7 days in. [score:1]
Finally, in the miR-365 NC group, the rats were injected with 10 μL morphine in the morning and afternoon every day for seven days and were injected with 10 μL of miR-365 NC (5’-UUCUCGAACGUGUCACGUUUU-3′) before morphine administration in the morning. [score:1]
Intrathecal injection of mir365 significantly increased the maximal possible analgesic effect (%MPE) in morphine tolerant rats. [score:1]
The key objective of the present study was to evaluate the effects of miR-365 on morphine analgesic tolerance by targeting β-arrestin2 in a rat mo del of morphine tolerance. [score:1]
Moreover, previous studies have demonstrated that the induction of miR-365 may potentially represent a vicious gateway that results in the abnormal release of TNFα [32]. [score:1]
The rats in the miR-365 mimic group were injected with 10 μL morphine in the morning and afternoon every day for seven days in addition to being injected with 10 μL of miR-365 mimics (5’-UAAUGCCCCUAAAAAUCCUUAU-3′) before morphine administration in the morning. [score:1]
Fig. 1The %MPE of rats in each group after administration at 0 d, 1 d, 3 d, 5 d and 7 d. Note: A, line graph of %MPE in each group; B, AUC analyses of %MPE in each group; %MPE, percentage of the maximal possible analgesic effect; N = 8; [*], P < 0.05 compared with the control group; [#], P < 0.05 compared with the morphine tolerance group; AUC, area under the curve; NC, negative control was employed to verify the targeting relationship between miR-365 and β-arrestin2. [score:1]
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4
[+] score: 32
As a result, five up-regulated miRNAs (miR-874-3P, miR-20a-5p, miR-345-3p, miR-365-5p and miR-764-3p) and one down-regulated miRNA (miR-99b-3p) were screened out for subsequent qRT-PCR confirmation. [score:7]
The levels of six differentially expressed miRNAs (miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p and miR-99b-3p) in the rat hippocampus at 24 hours after SE were confirmed using qRT-PCR. [score:3]
More importantly, we found that the expression of miR-365-5p and miR-99b-3p were significantly correlated with neuronal apoptosis after SE. [score:3]
However, the expression of miR-874-3p, miR-345-3p, miR-365-5p, and miR-764-3p were found to be increased in our study, whereas the levels of these four miRNAs stayed unchanged in study from Risbud et al. These differences might attribute to different SE mo dels, experimental methods as well as the criteria for miRNA screening in these two studies. [score:3]
0078375.g002 Figure 2The levels of six differentially expressed miRNAs (miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p and miR-99b-3p) in the rat hippocampus at 24 hours after SE were confirmed using qRT-PCR. [score:3]
The expression of miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p and miR-764-3p were significantly increased at 24 hours after SE (P<0.05), peaked at 1 week (P<0.05) and returned to the basal levels at 3 weeks after SE (Figure 3A-3E). [score:3]
As shown in Figure 2, the expression of miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p was significantly increased after SE (P<0.05), whereas the levels of miR-99b-3p was markedly decreased (P<0.05). [score:3]
After analyzing the initial results of deep sequencing, six deferentially expressed miRNA (miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p and miR-99b-3p) were screened out based on the criteria mentioned in, and qRT-PCR was performed to confirm their alterations after SE. [score:3]
Correlations between levels of miR-365-5p and miR-99b-3p and apoptosis index. [score:1]
More importantly, miR-365-5p and miR-99b-3p have been revealed to be significantly correlated with neuronal apoptosis. [score:1]
Pearson's correlation analysis suggested a positive correlation between miR-365-5p and apoptosis index (Figure7A and 7B, CA1: R = 0.925, P = 0.008; CA3: R = 0.877, P = 0.0218). [score:1]
0078375.g007 Figure 7(A,B) The correlation between miRNA-365-5p and apoptosis index in the CA1 and CA3 regions after SE. [score:1]
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[+] score: 19
For example, miR-324-5p, miR-365 localized on chromosome 10 and miR-153 and miR-203 localized on chromosome 6 showed significant upregulation. [score:4]
[67] On the other hand, MECP2, a transcriptional regulator targeted by miR-19, miR-30e and miR-365, binds to methylated DNA and has been shown to contribute to early life stress -dependent epigenetic programming of HPA axis -associated genes. [score:4]
[63] A large number of cyclic AMP-specific PDEs are also targets of multiple miRNAs (miR-101a, miR-124, miR-721, miR-137, miR-19b, miR-30e, miR-365). [score:3]
[50] MiR-101a, miR-124, miR-721, miR-181c and miR-365 target ERK/MAPK1, a gene involved in several physiological functions in brain including cell proliferation, differentiation and cell survival. [score:3]
As listed in Supplementary Table 6, these genes were predicted targets of miR-124, miR-101, miR-29a, miR-30e, miR-181c, miR-365 and miR-218. [score:3]
For example, miR-218, miR-324-5p, miR-365 and miR-146a were localized on chromosome 10; miR-764-5p and miR-351 on chromosome X; miR-101 and miR-30e on chromosome 5; miR-582 and miR-137 on chromosome 2; miR-153 and miR-203 on chromosome 6; miR-124 and 181a on chromosome 3 and miR-135a*/miR-135a-3p and let-7i on chromosome 7. Some of the miRNAs that were localized on the chromosome and in close proximity showed the same direction of changes. [score:2]
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[+] score: 14
On the one hand, previous studies have suggested that let-7 can suppress the expression of MOR [43], and our previous results suggest miR-365 can modulate morphine tolerance by targeting the beta-arrestin 2 protein [11]. [score:7]
According to the ceRNA analysis, we obtained an overview of the potential lncRNA /miRNA/mRNA interactions (Fig.   4a), and we then further identified several promising networks of lncRNA/miRNA/mRNA interactions (Fig. 4b), which included (MRAK161211, MRAK150340)/miR-219b/Tollip and XR_006440/(miR-365, let7)/(Usp31, Usp42, Clcn4–2) networks, and we used these networks to create functional annotations of the predicted target mRNAs by searching the Gene database. [score:3]
Among ncRNAs, some studies have reported that miRNAs are involved in the development of morphine tolerance [7, 8], including the let-7 family, miR-23b [9], miR-133b, miR-339 [10], miR-365 [11] and miR-219-5p [12]. [score:2]
In our study, we found that several possible interacting pathways among ceRNAs exist, including the following: MRAK161211, MRAK150340/miR-219b/mRNAs (e. g., Tollip, and Ubqln4); XR_006440/miR-365, let7/mRNAs (e. g., Usp31, Usp42, Clcn4–2); and MRAK161211/miR-133/Usp13. [score:1]
Therefore, the XR_006440/(let7, miR-365)/(Usp31, Usp42) pathway is likely to be responsible for the formation of morphine tolerance. [score:1]
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[+] score: 7
However, Nurr1 expression is not regulated by miR-365-3p. [score:4]
Eleven miRNAs, including miR-145-5p, miR-34c-5p, miR-365-3p, miR-214-3p, miR-151, miR-27a, miR-153-5p, miR-365-3p, miR-33-5p, miR-217-5p and miR-129-5p, were differentially and significantly expressed (P < 0.05; Figure 2B). [score:3]
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[+] score: 4
miR-365 is the first identified mechanically responsive miRNA in chondrocytes, which regulates chondrocyte differentiation through inhibiting HDAC4 [33]. [score:4]
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[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
MiR-145 and miR-365 were specifically expressed in DRG (Fig. 3a). [score:3]
Dorsal root ganglion let-7c, miR-17, miR-145, miR-150, miR-199a, miR-223, miR-365, miR-451. [score:1]
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[+] score: 4
Yang X Mechanical and IL-1beta responsive miR-365 contributes to osteoarthritis development by targeting histone deacetylase 4Int. [score:4]
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11
[+] score: 2
In a previous study, we demonstrated the deregulation of nine different miRNAs in rat spinal cord after chronic morphine injection, including let-7, miR-365 and miR-219-5p (miR-219) [4]. [score:2]
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[+] score: 2
analysis confirmed the direction and amplitude of all miRNA changes with the exception of let-7d, miR-25*, miR-187, miR-291a-5p, miR-292-5p, miR-365, miR-431, miR-487b, miR-615-5p, miR-743a, miR-20b-3p, miR-199a-3p which remained unaltered or showed no statistical significance. [score:2]
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[+] score: 1
It was found that miR-494, miR-365 and miR-451 were present in liver, miR-206, miR-468 and miR-691 in spleen, and miR-223, miR-98 and miR-206 in lung. [score:1]
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