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8 publications mentioning rno-mir-187

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-187. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 231
Other miRNAs from this paper: rno-mir-34a, rno-mir-98, rno-mir-146a, rno-mir-155
We observed that IL-10 secretion and miR-187 expression levels are inversely correlated after SE, in which IL-10 expression was highest in the chronic phase, when expression of miR-187 was at its lowest level; miR-187 expression was highest in the latent phase, when IL-10 expression was at its lowest level. [score:11]
In addition, we examined the effect of modulation of IL-10 expressions on miR-187 expressions in vitro on the neuron level and the effect of antagonizing miR-187 on the expression of IL-10 to identify the correlation between miR-187 and IL-10 expression levels. [score:9]
This significant decrease in miR-187 expression which is associated with the significant increased level of IL-10 expression in this animal mo del support the hypothesis that miR-187 may represent an attempt to regulate the anti-inflammatory response of IL-10 by inducing its expression level (Rossato et al., 2012). [score:8]
qPCR results showed significant downregulation of miR-187 expression in the rat hippocampal tissues in the latent and chronic phases of TLE development ([*] p < 0.05). [score:7]
Therefore, the dramatic downregulation of miR-187 expressions in both rat mo dels and patients with TLE during epileptogenesis and chronic phase indicates their underlying functions in the process of TLE development. [score:7]
Interestingly, miR-187 exhibited an opposite expression manner to IL-10 which was significantly downregulated during the latent and chronic phases of TLE development in a gradual manner. [score:7]
In the chronic phase, miR-187 expression reached its lowest, which was confirmed by its downregulation in patients with TLE. [score:6]
Kretschmann et al. (2015) found a significant downregulation of miR-187 expression at 28 days pilocarpine -induced SE in mice. [score:6]
A dramatically downregulation of miR-187 in the neurons was detected after treatment with LPS + IL-10 than control neurons, while simultaneous addition of anti-IL-10 Ab to LPS-stimulated neurons restored the expression of miR-187 (Data are presented as the mean ± SD, [*] p < 0.05; n = 5/group). [score:6]
qPCR results showed also significant downregulation of miR-187 expression in the hippocampal tissue of TLE patients relative to controls ([*] p < 0.05). [score:6]
qPCR results revealed a significant downregulation in miR-187 expression in the neurons after stimulation with LPS than controls ([*] p < 0.05). [score:6]
miR-187 expression failed to be downregulated when IL-10 is blocked with anti–IL-10 antibody. [score:6]
Furthermore, simultaneous addition of IL-10 to LPS-stimulated neurons suppressed the expression of miR-187 compared to LPS-stimulated neuron group, whereas simultaneous addition of anti-IL-10 Ab to LPS-stimulated neurons restored the expression of miR-187 (Figure 3). [score:6]
Briefly, miR-187 expression in rat hippocampus following SE was antagonized using an antagomir that specifically and efficiently targets miR-187. [score:5]
Stimulation of the neurons with LPS leads to a significant downregulation of miR-187 expression compared to the resting state. [score:5]
In the acute phase, miR-187 expression was almost equal to expression values in the control group. [score:5]
The current study shows that IL-10 and miR-187 are mediated in the pathogenesis of TLE development and their opposite expression patterns in the phases of TLE development may suggest an interactive relationship between the two markers, suggesting that miR-187 may play a critical role in the modulation of the neuroinflammatory response during the pathogenesis of TLE. [score:5]
In the present study, we first demonstrated an association between IL-10 as an anti-inflammatory cytokine and miR-187 as a post-transcriptional inflammation- related miRNA during the three phases of TLE development in a rat mo del, and we confirmed our results by detecting their expressions in patients with TLE, which are equal to the chronic phase in the rat mo del. [score:4]
The latent phase statistically reduced the expression of miR-187 compared to normal controls and its expression being more decreased in 21 days than in 7 days group. [score:4]
In association with our observation, several profiling studies have shown that miR-187 is downregulated in the chronic phase of TLE either in experimental mo dels or patients with TLE. [score:4]
The aim of the present study was to detect the dynamic expression of IL-10 as anti-inflammatory cytokine and miR-187 as a post-transcriptional inflammation-related miRNA in the hippocampus of rats following pilocarpine -induced status epilepticus (SE) during the three phases of TLE development and in patients with TLE. [score:4]
Figure 2 (A) miR-187 relative dynamic expression in the three phases of TLE development in a rat mo del. [score:4]
These results are supported by findings that suggest a major role for miR-187 in the physiological regulation of IL-10–driven anti-inflammatory responses by inhibiting several proinflammatory cytokins production including TNF-α, IL-6 and IL-12p40 (Rossato et al., 2012). [score:4]
In their study, they also evaluated the prolonged expression of miR-187 in tissues collected from different time points (7–90 days post-SE) which was also downregulated. [score:4]
Therefore, downregulation of miR-187 in response to LPS may be required for proper IL-10 production during TLE. [score:4]
Figure 3 qPCR results showed a significant downregulation of miR-187 in the neurons after treatment with LPS than control neurons. [score:4]
miR-187 Expression in Rats During the Three Phases of TLE Development. [score:4]
miR-187 Expression by qPCR in the Hippocampi of Rats, and TLE Patients. [score:3]
On the other hand, antagonizing of miR-187 function by antagomir in the post-SE rat hippocampus significantly increased the expression levels of IL-10 after antagonizing miR-187. [score:3]
Effect of miR-187 Antagomir in IL-10 Expression Level. [score:3]
Several lines of evidence clearly point to the requirement for IL-10 in the reduction of miR-187 expression in LPS-activated neurons. [score:3]
Effect of Modulation of IL-10 on miR-187 Expression in the Neurons. [score:3]
Therefore, modulation of the IL-10/miR-187 axis may be a novel therapeutic target for TLE. [score:3]
IL-10 alone has been shown to be a relatively weak stimulus, but it strongly synergized with LPS in alteration of miR-187 expression (Rossato et al., 2012). [score:3]
While in the stimulated group, neurons were cultured without serum Neurobasal-B-27 medium for 6 h and then with Neurobasal-B-27 medium and one or more of the following reagents alone or in combination: recombinant rat IL-10 200 U/mL (abnova), anti-rat IL-10 monoclonal antibody 1 μg/mL (Clone 2G101H7; Biocompare), and LPS 100 ng/mL derived from Escherichia coli (Sigma) for 24 h to explore the effect of IL-10 stimulation on miR-187 expression. [score:3]
At 7 days following SE onset, rats were decapitated under deep anesthesia using chloral hydrate (10%, 5 ml/kg, i. p. ) and hippocampal tissue was quickly removed for detection of miR-187 expression and detection of its critical downstream molecules IL-10. [score:3]
miR-187 Expression in Patients with TLE. [score:3]
Furthermore, we explored the effect of antagonizing of miR-187 in IL-10 expression levels. [score:3]
Thus, miR-187 mediated posttranscriptional control could be involved in fine tuning the requirement level of IL-10 expression in anti-inflammatory responses following SE. [score:3]
In the tissues obtained from patients, miR-187 expression was normalized to rnu6b (Figure 2B). [score:3]
qPCR results showed that IL-10 expression level is increased at 7 days post-SE in the rat hippocampal tissues both before and after miR-187 antagomir/antagomir-control treatments. [score:3]
In rat tissues, miR-187 expression was normalized to that of the U6B small nuclear RNA gene (rnu6b; Figure 2A). [score:3]
miR-187 expression was normalized to that of the rnu6b. [score:3]
In the control group, neurons were cultured without serum Neurobasal-B-27 medium for 30 h to explore the expression of miR-187 on the resting neurons. [score:3]
Several studies have suggested a link between miR-187 and chronic human inflammatory diseases (Holliday et al., 2011; Guardia et al., 2013; Suojalehto et al., 2014). [score:3]
In the acute phase no significant deregulation was detected in both IL-10 and miR-187. [score:2]
Furthermore, IL-10 directly abolished LPS-reduced miR-187 transcription, which is potentiated in the presence of IL-10–blocking antibodies. [score:2]
Recently, miR-187 has been implicated in the regulating of immune and inflammatory processes (Guardia et al., 2013; Suojalehto et al., 2014). [score:2]
These data point to miR-187 as a LPS-related miRNA up regulated by IL-10. [score:2]
The expression of IL-10 protein at 7 days post-SE in the rat hippocampus increased in the miR-187 antagomir -treated group when compared with the antagomir-control -treated group (Figure 4B). [score:2]
Furthermore, miR-187 negatively regulates several proinflammatory cytokines production produced by primary human monocytes (Rossato et al., 2012). [score:2]
Stimulation of IL-10 expression level was markedly observed in the miR-187 antagomir group compared to the antagomir-control -treated group (Figure 4A). [score:2]
IL-10 -induced microRNA-187 negatively regulates TNF-α, IL-6 and IL-12p40 production in TLR4-stimulated monocytes. [score:2]
Notably, several profiling studies have shown that miR-187 is not deregulated in the acute phase of TLE (Hu et al., 2011, 2012), which coincides with our findings in this study. [score:2]
Figure 4 The results of the miR-187 antagomir experiment. [score:1]
McKiernan et al. (2012) found that mature miR-187 was decreased in association with dicer loss in patients with TLE and HS. [score:1]
A miR-187 antagomir or an antagomir-control (Ribo-Bio Co. [score:1]
miR-187 Antagomir Experiments. [score:1]
Overall, our observations represent evidence that miR-187 are strongly involved in the anti-inflammatory functions of IL-10 during TLE. [score:1]
The relative expression level for miR-187 was calculated using the comparative CT method. [score:1]
This suggests that miR-187 may play a special role in the pathogenesis of TLE. [score:1]
Another study by Gorter et al. (2014) also detected a significant decreased of miR-187 at 3–4 months following SE induced by electrical stimulation of angular bundle in rats. [score:1]
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2
[+] score: 26
In these 10 deregulated miRNAs, seven (let-7d*, miR-181b, miR-187, miR-214, miR-466b, miR-592, miR-1224) are up-regulated in two rats, and one (miR-195) is down-regulated. [score:8]
Amongst these, miR-383 was differentially expressed in all three rats and up-regulated to the largest degree in rat one, and the ten other miRNAs, let-7d*, miR-181b, miR-187, miR-195, miR-214, miR-382, miR-411, miR-466b, miR-592 and miR-1224 were differentially expressed in at least two rats. [score:8]
In dysregulated miRNAs, let-7d*, miR-181b, miR-187, miR-214, miR-383, miR-466b, miR-592, miR-1224 are significantly overexpressed in MrD compared to hippocampus, and miR-195 is downexpressed. [score:5]
Hence, miR-383 was differentially expressed in three rats, and let-7d*, miR-181b, miR-187, miR-195, miR-214, miR-382, miR-411, miR-466b, miR-592, miR-1224 were differentially expressed in two rats at least (Additional file 2: Table S4). [score:5]
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3
[+] score: 6
The largest decreases in expression were observed in miR-187-3p, miR-551b-3p and miR-7a-5p at 0.61, 0.67 and 0.71 fold of the control levels respectively. [score:3]
The largest decrease in expression was observed in miR-7a-5p, miR-551b-3p and miR-187-3p at 0.53, 0.56 and 0.56-fold of the control, respectively. [score:3]
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4
[+] score: 5
Other miRNAs from this paper: rno-mir-31a, rno-mir-221
Interestingly, except for miRNAs rno-miR-187 and -181a, miRNA expression changes induced by overexpression of HO-1 43 differed from those found in ammonia exposed astrocytes in the present study (data not shown). [score:5]
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5
[+] score: 4
MicroRNAs like miR-19a, 34b, 129, 135a, 142-3p, miR-153, miR-186, miR-187, and miR-301a were significantly downregulated in Cs1-ko mice. [score:4]
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6
[+] score: 4
rno-miR-881, rno-miR-880, miR-741-3p, miR-511*, miR-187, miR-449a, as well as 6 members of miR-34 family, miR-34a, miR-34a*, miR-34b, miR-34b*, miR-34c, and miR-34c*, showed over 10-fold up-regulation. [score:4]
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7
[+] 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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8
[+] score: 1
For example, nine miRNAs (miR-21, miR-20a, miR-146a, miR-199a-3p, miR-214, miR-192, miR-187, miR-805, and miR-194) have been identified in C57BL/6 mice as promising biomarkers of kidney injury after renal ischemia reperfusion injury (IRI) [15]. [score:1]
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