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10 publications mentioning rno-mir-382

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-382. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 455
To determine the biological functions of miR-382, its expression is up-regulated by adenovirus expressing miR-382 (Ad-miR-382) or pre-miR-382, but is down-regulated by its special antisense oligonucleotide (LNA-anti-miRNA-382). [score:11]
Drd1 is a direct target gene of miR-382 and is a regulator for the expression of DeltaFosBAlthough miR-382 has a strong regulatory effect on the expression of DeltaFosB, computational analysis failed to find any binding sites for miR-382 in its mRNA sequence. [score:10]
miR-382 expression in rat NAc was down-regulated by LNA-anti-miR-382 (Anti-miR-382) (p = 0.00133), but was up-regulated by Ad-miR-382 (p = 0.00102). [score:9]
The expression of miR-382 in rat NAc was down-regulated via its specific antisense, the locked-nucleic-acid -modified antisense oligonucleotide for miR-382 (LNA-anti-miRNA-382), and was up-regulated via Ad-miR-382. [score:9]
In this experiment, LNA-anti-miR-382 was used to knock-down its expression and Ad-miR-382 was used to up-regulate its expression. [score:9]
miR-382 expression was down-regulated by LNA-anti-miR-382 (p = 5.08726615734E-5), but was up-regulated by pre-miR-382 (p = 1.69645597989E-5). [score:9]
Overexpression of miR-382 is sufficient to inhibit alcohol -induced up-regulation of DRD1 and DeltaFosB in rat NAc: * p < 0.01, ** p < 0.001, ## p < 0.001, Student's t-test. [score:8]
Moreover, the alcohol -mediated up-regulation of DRD1 and DeltaFosB was significantly inhibited by overexpression of miR-382. [score:8]
Moreover, overexpression of miR-382 significantly attenuates alcohol -induced upregulation of DRD1 and DeltaFosB, decreases voluntary intake of and preference for alcohol, and inhibits the DRD1 -induced action potential responses. [score:8]
Figure 4Overexpression of miR-382 is sufficient to inhibit alcohol -induced up-regulation of DRD1 and DeltaFosB in rat NAc: * p < 0.01, ** p < 0.001, ## p < 0.001, Student's t-testSource data is available for this figure in the Supporting Information. [score:8]
Overexpression of miR-382 via adenovirus -mediated gene transfer is sufficient to inhibit alcohol -induced up-regulation of the DRD1 and DeltaFosB in rat NAc. [score:8]
Drd1 is a direct target gene of miR-382 and is a regulator for the expression of DeltaFosB in cultured CAD cells: ** p < 0.01, *** p < 0.001, Student's t-test. [score:7]
Figure 3 Drd1 is a direct target gene of miR-382 and is a regulator for the expression of DeltaFosB in cultured CAD cells: ** p < 0.01, *** p < 0.001, Student's t-test Source data is available for this figure in the Supporting Information. [score:7]
As shown in Fig 2, miR-382 level in rat NAc was successfully down-regulated by LNA-anti-miR-382 (n = 4, t-test, p = 0.00133), but was up-regulated by Ad-miR-382 (n = 4, t-test, p = 0.00102). [score:7]
Drd1 is a direct target gene of miR-382 and is a regulator for the expression of DeltaFosB. [score:7]
Downregulation of DRD1 and DeltaFosB via overexpression of miR-382 in NAc. [score:6]
Overexpression of miR-382 via Ad-miR-382 prevented alcohol -induced up-regulation of DRD1 (## p = 0.0002) and DeltaFosB (## p = 0.00012) in rat NAc. [score:6]
This experiment is for answering an important question: whether or not the alcohol -induced up-regulation of DRD1 and DeltaFosB can be prevented by overexpression of miR-382. [score:6]
To further confirm that Drd1 is a direct target gene in neuronal cells, the expression of miR-382 in cultured CAD cells was modulated by LNA-anti-miR-382 (n = 5, t-test, p = 5.08726615734E-5) and pre-miR-382 (n = 5, t-test, p = 1.69645597989E-5) (Fig 3). [score:6]
Alcohol down-regulates the expression of miR-382 in rat NAc. [score:6]
Via this target gene, miR-382 strongly modulates the expression of another alcohol-related signal molecule, DeltaFosB. [score:5]
Generation of the adenovirus expressing miR-382 (Ad-miR-382) and control adenovirus expressing GFP (Ad-GFP). [score:5]
Representative Western blots of DRD1 and DeltaFosB from animals treated with vehicle, anti-control or Anti-miR-382 were shown in Fig 2. In contrast, overexpression of miR-382 via Ad-miR-382 decreased the expression of DRD1 (n = 6, t-test, p = 0.00041) and DeltaFosB (n = 6, t-test, p = 0.00087) (Fig 2). [score:5]
Among them, miR-382 is an important regulator and participator in alcohol intake via its direct target gene Drd1 and its downstream signal molecule DeltaFosB. [score:5]
Our microarray data revealed that miR-382 is an abundant miRNA in NAc and its expression was down-regulated after 7-days alcohol injection (n = 9, t-test p = 1.93E-10, compared with that in vehicle -treated controls) (Fig 1). [score:5]
Overexpression of miR-382 via Ad-miR-382 decreased the expression of DRD1 (p = 0.00041) and DeltaFosB (p = 0.00087) in rat NAc. [score:5]
However, the alcohol -induced up-regulation of DRD1 (n = 5, t-test, p = 0.0002) and DeltaFosB (n = 5, t-test, p = 0.00012) was prevented by the overexpression of miR-382 (note: Alcohol + Ad-miR-382 group compared with Alcohol + Ad-GFP group) (Fig 4). [score:5]
Then, these HEK 293 cells were treated with vehicle, pDNR-CMV (an empty plasmid, 0.2 µg/ml), pmiR-382 (a plasmid expressing miR-382, 0.2 µg/ml) or pmiR-31 (a plasmid expressing miR-31, 0.2 µg/ml). [score:5]
We found that overexpression of miR-382 in rat NAc via adenovirus -mediated gene transfer is sufficient to inhibit the voluntary intake of and preference for alcohol in these rats. [score:5]
Among them, miR-382 is an important regulator and participator in alcohol intake via its direct target gene Drd1 and its downstream signal molecule DeltaFosB. [score:5]
Overexpression of miR-382 via Ad-miR-382 is sufficient to inhibit the voluntary intake of and the preference for alcohol in rats under the intermittent access two-bottle choice drinking paradigm. [score:5]
Overexpression of miR-382 is sufficient to inhibit the voluntary intake of and the preference for alcohol in rats: the animals (total n = 24) under the intermittent access two-bottle choice drinking paradigm were randomly divided into three groups which received infusion of Ad-miR-382, control adenovirus Ad-GFP or vehicle (saline), respectively, into the NAc. [score:5]
was performed to test whether or not the miR-382 could bind to and inhibit Drd1expressioin. [score:5]
Figure 5Overexpression of miR-382 is sufficient to inhibit the voluntary intake of and the preference for alcohol in rats: the animals (total n = 24) under the intermittent access two-bottle choice drinking paradigm were randomly divided into three groups which received infusion of Ad-miR-382, control adenovirus Ad-GFP or vehicle (saline), respectively, into the NAcSeven days later, the rats were allowed to resume ethanol consumption under the same drinking paradigm. [score:5]
Among them, miR-382 is down-regulated by about 50% in alcohol -treated rats. [score:4]
Catecholaminergic neuronal cell (CAD cell) culture, the expression modulation of miR-382 and knockdown of DRD1. [score:4]
The successful up-regulation of miR-382 via Ad-miR-382 was verified by qRT-PCR (n = 3, t-test, p = 0.00125) (Fig 6). [score:4]
DRD1 and DeltaFosB are two critical molecules related to alcohol abuse as described in Section 1. Our computational analysis and experimental approach have demonstrated that Drd1 might be a direct target gene of miR-382. [score:4]
The aim of this study is to determine the expression profile of miRNAs in the nucleus accumbens (NAc) of rats treated with alcohol, and the role of an alcohol-regulated miR-382 in alcohol intake as well as the potential molecular mechanisms involved. [score:4]
For the miR-382 up-regulation, pre-miR-382 (Ambion, Inc. ) [score:4]
Although miR-382 has a strong regulatory effect on the expression of DeltaFosB, computational analysis failed to find any binding sites for miR-382 in its mRNA sequence. [score:4]
The successful up-regulation of miR-382 via Ad-miR-382 was verified by qRT-PCR (n = 3, t-test, p = 0.00076) (Fig 4). [score:4]
Luciferase assay was performed to test whether or not the miR-382 could bind to and inhibit Drd1expressioin. [score:4]
Thus, DeltaFosB might not be a direct target gene of miR-382. [score:4]
Both gain-of-function and loss-of-function approaches have demonstrated that miR-382 was a strong regulator for the expression of both DRD1 and DeltaFosB in rat NAc. [score:4]
The successful up-regulation of miR-382 via Ad-miR-382 was verified by qRT-PCR at 7 days after alcohol drinking (Supporting Information Fig S2). [score:4]
The successful up-regulation of miR-382 via Ad-miR-382 was verified by qRT-PCR at 7 days after drinking (Supporting Information Fig S1). [score:4]
In both cultured neuronal cells in vitro and in the brain NAc in vivo, we have identified that the dopamine receptor D1 (DRD1), an alcohol addiction-related signal molecule, is a direct target gene of miR-382. [score:4]
Among them, miR-382 is down-regulated in alcohol -treated rats. [score:4]
The result indicates that DeltaFosB might not be a direct target gene for miR-382. [score:4]
Regulation of the miR-382 expression in rat NAc via microinjection. [score:4]
The result suggests Drd1 might be a potential direct target gene of miR-382. [score:4]
At the protein level, we found that pre-miR-382 decreased the expression of DRD1 (n = 5, t-test, p = 2.44969469509E-5) and DeltaFosB (n = 5, t-test, p = 0.0008). [score:3]
A-C. The successful modulation of miR-382 expression by Ad-miR-382. [score:3]
The expression of miR-382 in the nucleus accumbens (NAc) of rats after treatment with alcohol: 18 male rats were treated with vehicle (500 µl saline, i. p. bid) or alcohol (1 g/kg, i. p. bid). [score:3]
The expression of miR-382 in cultured CAD cells was modulated by LNA-anti-miR-382 (Anti-miR-382) and pre-miR-382. [score:3]
To test the effects of miR-382 on the expression of DRD1 and DeltaFosB, both gain-of-function and loss-of-function approaches were applied. [score:3]
Representative Western blots of DRD1 and DeltaFosB from animals treated with vehicle or alcohol were shown in Fig 2. Figure 2The effect of miR-382 on the expression of DRD1 and DeltaFosB in rat NAc: ** p < 0.01, *** p < 0.001, Student's t-test Source data is available for this figure in the Supporting Information. [score:3]
In addition, the injected-Ad-miR-382 increased miR-382 expression in NAc, but not in the neighbouring brain areas (Supporting Information Fig S1). [score:3]
To determine the potential role of miR-382 in alcohol intake, the effect of miR-382 on the expression of DRD1 and DeltaFosB in rat NAc was determined. [score:3]
n = 9, p = 6.53E-9. To determine the potential role of miR-382 in alcohol intake, we determined the effect of miR-382 on the expression of DRD1 and DeltaFosB in rat NAc. [score:3]
The construct with mutated fragment of the 3′-UTR of Drd1 mRNA without the putative miR-382 binding sequences was used as the mutated control (mutated Drd1), pmiR-382, but not pmiR-31 or pDNR-CMV, inhibited luciferase activity (p = 1.17571599413E-6). [score:3]
Ad-miR-382 increased the expression of miR-382 in NAc of rats with alcohol administration (p = 0.00079). [score:3]
As shown in Fig 3, miR-382 indeed could inhibit the luciferase activity (n = 6, t-test, p = 1.17571599413E-6). [score:3]
Ad-miR-382 increased the expression of miR-382 in NAc of rats (p = 0.00125). [score:3]
Although DRD1 was still expressed at very low level in miR-382-overexprssed NAc, the changes in excitability of NAc MSNs caused by DRD1 activation had been completely blocked. [score:3]
In the mutated control group, the inhibitory effect of pmiR-miR-382 on luciferase activity disappeared. [score:3]
At protein level, pre-miR-382 decreased the expression of DRD1 (p = 2.44969469509E-5) and DeltaFosB (p = 0.0008). [score:3]
In the mutated control group, the inhibitory effect of miR-382 on luciferase activity in HEK 293 cells disappeared (Fig 3). [score:3]
Figure 6Overexpression of miR-382 influences responses of MSNs in NAc slices to DRD1 activation: 4 µl of vehicle, Ad-GFP or Ad-miR-382 (1 × 10 [9] pfu/ml) was infused into the NAc of rats Severn days later, the NAc were isolated. [score:3]
Interestingly, the expression of DRD1 (n = 6, t-test, p = 0.00057) and DeltaFosB (Fig 2) (n = 6, t-test, p = 0.0004) in rat NAc was significantly increased by the LNA-anti-miR-382. [score:3]
At the mRNA level, we also found that pre-miR-382 decreased, whereas Anti-miR-382 increased the expression of Drd1 (n = 5, t-test, p = 0.00416 and n = 5, t-test, p = 0.00039) and DeltaFosB (n = 5, t-test, p = 7.21292762637E-5 and n = 5, t-test, p = 0.00027) (Fig 3). [score:3]
Drd1 is a potential target gene of miR-382 predicted by computational analysis. [score:3]
In contrast, the expression of DRD1 (p = 0.00089) and DeltaFosB (p = 0.00149) was increased by LNA-anti-miR-382 (Anti-miR-382). [score:3]
Overexpression of miR-382 influences responses of MSNs in NAc slices to DRD1 activation. [score:3]
Second, although miR-382-DRD1 is a critical pathway for DRD1 -mediated effect on MSN firing, miR-382 may also have other unidentified targets that could also affect the DRD1 agonist -mediated effect on MSN excitability. [score:3]
pre-miR-382 decreased, whereas Anti-miR-382 increased the expression of Drd1 (p = 0.00416 and 0.00039) and DeltaFosB (p = 7.21292762637E-5 and 0.00027) at mRNA level. [score:3]
The luciferase reporter construct, containing the putative miR-382 binding sequence from 3′-UTR of rat Drd1 gene, was transfected into HEK293 cells with vehicle (Vehicle), an empty vector (pDNR-CMV), miR-382 (pmiR-31) or a control plasmid expressing an unrelated miRNA, miR-31 (pmiR-31). [score:3]
Representative Western blots of DRD1 and DeltaFosB from animals treated with vehicle or alcohol were shown in Fig 2. Figure 2The effect of miR-382 on the expression of DRD1 and DeltaFosB in rat NAc: ** p < 0.01, *** p < 0.001, Student's t-test Source data is available for this figure in the Supporting Information. [score:3]
Based on the results, we hypothesize that DRD1 might be an upstream signal molecule for DeltaFosB and miR-382 -mediated effect on the expression of DeltaFosB might be induced by DRD1. [score:3]
Ad-miR-382 and Ad-GFP were generated using ViraPower™ Adenoviral Gateway Expression system (Invitrogen, CA) according to the manufacturer's protocols as described previously (Cheng et al, 2009). [score:3]
The expression of DRD1 (p = 0.00057) and DeltaFosB (p = 0.0004) in rat NAc was increased by LNA-anti-miR-382. [score:3]
In contrast, the expression of DRD1 (n = 5, t-test, p = 0.00089) and DeltaFosB (n = 5, t-test, p = 0.00149) was increased by LNA-anti-miR-382 (Anti-miR-382) (Fig 3). [score:3]
XL was responsible for the adenovirus expressing miR-382 and GFP. [score:3]
This experiment was to determine whether the changes of miR-382 expression in the NAc could affect the drinking behaviour. [score:3]
Alcohol decreased the expression of miR-382 in rat NAc (p = 0.00076). [score:3]
Overexpression of miR-382 influences responses of MSNs in NAc slices to DRD1 activation: 4 µl of vehicle, Ad-GFP or Ad-miR-382 (1 × 10 [9] pfu/ml) was infused into the NAc of rats. [score:3]
The successful modulation of miR-382 expression by Ad-miR-382. [score:3]
The effect of miR-382 on the expression of DRD1 and DeltaFosB in rat NAc: ** p < 0.01, *** p < 0.001, Student's t-test. [score:3]
Among them, miR-382 was found to be down regulated by about 50% after treatment with alcohol. [score:2]
miR-382 is a critical regulator for the signal molecules, DRD1 and DeltaFosB, in rat NAc. [score:2]
For the miR-382 knockdown, LNA-anti-miR-382 was added to the culture media at final oligonucleotide concentration of 50 nM. [score:2]
Representative Western blots of DRD1 and DeltaFosB from animals treated with vehicle, Ad-GFP or Ad-miR-382 were shown in Fig 2. The results suggested that miR-382 is a critical regulator for both DRD1 and DeltaFosB in rat NAc. [score:2]
While the application of 1 µM SKF38393, the DRD1 agonist increased the firing rate of the MSN of rats that received saline injection, this was not seen in rats received Ad-miR-382 injection. [score:1]
To determine the potential cellular modifications via miR-382 that could cause its behavioural effects, male rats (n = 12) were randomly divided into three groups (n = 4 for each) which received infusion of Ad-miR-382, control adenovirus Ad-GFP or vehicle, respectively, into the NAc as described above. [score:1]
The successful modulation of DRD1 and DeltaFosB via Ad-miR-382 was verified by at 7 days after alcohol drinking (Supporting Information Fig S3). [score:1]
However, the computational analysis failed to find any binding sites of miR-382 in the mRNA of DeltaFosB. [score:1]
We further demonstrate that miR-382 plays an important role in alcohol-seeking behaviour through the DRD1 and DeltaFosB pathway. [score:1]
As an internal control, U6 was used for miR-382 template normalization and GAPDH was used for DeltaFosB and Drd1 template normalization. [score:1]
miR-382 was decreased in alcohol -treated rats as determined by qRT-PCR. [score:1]
Interestingly, Ad-miR-382 did not significantly alter the water consumption (Fig 5) or the total fluid intake (Fig 5). [score:1]
The successful modulation of DRD1 and DeltaFosB via Ad-miR-382 was verified by at 7 days after drinking (Supporting Information Fig S2). [score:1]
LNA-anti-miR-382, Ad-miR-382 or their controls (vehicle, LNA-anti-miR-382 control, or Ad-GFP) was injected into the NAc via microinjection. [score:1]
Vehicle control, LNA-anti-miR-382 control, adenovirus control (Ad-GFP), LNA-anti-miR-382 or Ad-miR-382, was injected into the NAc via microinjection. [score:1]
The sequence of the LNA-anti-miR-382 is: 5′mCmGmAmAmUmCmCmAmCmCmAmCmGmAmAmCmAmAmCmUmUmC-3′. [score:1]
We next performed the computational analysis on Drd1 and found it has a miR-382 binding site at its 3′-UTR (Fig 3). [score:1]
Then, the animals were divided into the following groups: Vehicle -treated rats without alcohol administration (Vehicle); Ad-GFP -treated rats without alcohol administration (Ad-GFP); Ad-GFP -treated rats with alcohol administration (Alcohol + Ad-GFP) and Ad-miR-382 -treated rats with alcohol administration (Alcohol + Ad-miR-382). [score:1]
D. Summary graphs showing that Ad-miR-382 NAc injection attenuated the firing rate of MSNs–induced by 1 µM SKF38393 (p = 0.00654). [score:1]
Sample voltage traces in response to current injections (inset) from a MSN in acute brain slices of rats which received infusion of saline (B) and Ad-miR-382 (C), respectively. [score:1]
Then, the animals were divided into the following groups: vehicle -treated rats without alcohol administration (vehicle group); Ad-GFP -treated rats without alcohol administration (Ad-GFP group); Ad-GFP -treated rats with alcohol administration (Alcohol + Ad-GFP group) and Ad-miR-382 -treated rats with alcohol administration (Alcohol + Ad-miR-382 group). [score:1]
Three days before alcohol administration, 4 µl of vehicle, Ad-GFP or Ad-miR-382 (1 × 10 [9] pfu/ml) was infused into the NAc of rats. [score:1]
To verify this important discovery, we further determined the levels of miR-382 with the qRT-PCR technique. [score:1]
Ad-miR-382 did not alter the water consumption. [score:1]
Representative Western blots of DRD1 and DeltaFosB from animals treated with vehicle, Ad-GFP or Ad-miR-382. [score:1]
When rats maintained a stable baseline level of alcohol (ethanol) consumption (4.3 ± 0.2 g/kg/24 h) for 4 weeks (12 drinking sessions in total), they were randomly divided into three groups which received infusion of Ad-miR-382, control adenovirus Ad-GFP or vehicle (saline), respectively, into the NAc as described above. [score:1]
miR-382 was decreased in alcohol -treated rats as determined by microarray analysis. [score:1]
LNA-anti-miR-382 and its negative random oligonucleotide control (LNA-anti-miR-382 control) were synthesized by Integrated DNA Technologies. [score:1]
Vehicle control, and oligo controls for LNA-anti-miR-382 (LNA-anti-miR-382 control) and pre-miR-382 (pre-miR-382 control) were used as controls. [score:1]
The application of the DRD1 agonist of SKF38393 (1 µM) increased the action potential responses to current injection of the MSNs in rats that received NAc injections of either the control adenovirus Ad-GFP or the vehicle, but not in rats that received Ad-miR-382 injection (n = 4, two-way ANOVA, p = 0.00654) (Fig 6). [score:1]
The reporter plasmid, a firefly luciferase reporter construct psiCHECK-2 (Promega, WI) inserted with a fragment of the 3′-UTR of rat Drd1 mRNA containing the putative miR-382 binding sequence. [score:1]
At 3 days before alcohol administration, 4 µl of vehicle, Ad-GFP or Ad-miR-382 (1 × 10 [9] pfu/ml) was infused into the NAc of rats. [score:1]
The role of miR-382 in alcohol intake was determined in rats using an intermittent access two-bottle choice drinking paradigm. [score:1]
Ad-miR-382 decreased the preference for alcohol at all points (7 days: p = 0.0037; 9 days: p = 0.0041; 11 days: p = 0.0029; 13 days: p = 0.0015; 17 days: p = 0.0088; 19 days: p = 0.0068; 21 days: p = 0.018; 23 days: p = 0.0029). [score:1]
The reduction of alcohol intake started on the 7th day after Ad-miR-382 infusion into the NAc, and sustained during the 18-day period of observation (n = 8, two-way ANOVA, 7 days: p = 0.00039; 9 days: p = 0.00046; 11 days: p = 0.00057; 13 days: p = 0.00026; 17 days: p = 0.00018; 19 days: p = 0.00098; 21 days: p = 0.013; 23 days: p = 0.0035) (Fig 5). [score:1]
Ad-miR-382 did not alter the total fluid intake. [score:1]
The voluntary intake of alcohol was reduced via Ad-miR-382 at all points (7 days: p = 0.00039; 9 days: p = 0.00046; 11 days: p = 0.00057; 13 days: p = 0.00026; 17 days: p = 0.00018; 19 days: p = 0.00098; 21 days: p = 0.013; 23 days: p = 0.0035). [score:1]
Representative Western blots of DRD1 and DeltaFosB from animals treated with vehicle, anti-control or Anti-miR-382. [score:1]
After 18 alcohol access sessions, vehicle (4 µl saline), control adenovirus Ad-GFP (4 µl, 1 × 10 [9] pfu/ml) or Ad-miR-382 (4 µl, 1 × 10 [9] pfu/ml) was injected into rat NAc via microinjection as described. [score:1]
The above experiments indicate that miR-382 in the NAc has a particularly critical role in mediating the behavioural responses to alcohol. [score:1]
As illustrated in Fig 5, in the group which received Ad-miR-382, the voluntary intake of alcohol was significantly reduced, as demonstrated by the decreased overall main effect of treatment, main effect of day, and the significant treatment by day interaction on alcohol consumption. [score:1]
The construct with mutated fragment of the 3′-UTR of Drd1 mRNA without the putative miR-382 binding sequences was used as the mutated control. [score:1]
The vehicle (4 µl saline), LNA-anti-miR-382 (4 µl, 100 µM in 1% transfection reagent), LNA-LNA-anti-miR-382 control (4 µl, 100 µM in 1% transfection reagent), Ad-miR-382 (4 µl, 1 × 10 [9] pfu/ml) or the control virus (4µl, Ad-GFP) was injected bilaterally into NAc core with two 10 µl Hamilton syringe at a rate of 0.1 µl/min. [score:1]
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[+] score: 42
Of these ten, besides miR-382 and miR-411 which were up-regulated in one rat and down-regulated in another, the other eight miRNAs retained a uniform direction of regulation (up-regulation or down-regulation) between different specimens. [score:15]
Beside miR-382 and miR-411 which were up-regulated in one rat and down-regulated in another, the other nine miRNAs kept the uniform regulated direction (up or down) between different rats (Additional file 2: Table S4). [score:9]
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]
The last two investigated, miR-382 and miR-411, were up-regulated in one rat and down-regulated in another. [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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[+] score: 23
Of the 123 miRNAs, 15 were differentially expressed in the AS and CS mo del groups, of these, four were significantly upregulated (rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p; Table IV) and 11 were downregulated (significantly downregulated, rno-miR-135a and rno-miR-466b; Table V). [score:12]
Of these 15 miRNAs, rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p were significantly upregulated, particularly miR-296 (Table IV), and 11 were downregulated (miR-135a and miR-466b were significantly downregulated, particularly miR-135a; Table V). [score:10]
In conclusion, rno-miR-296, rno-miR-141, rno-miR-382, rno-miR-219-5p, miR-135a and miR-466b may be involved in stress at the molecular level, thus causing myocardial injury. [score:1]
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4
[+] score: 12
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-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, 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-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
Among the miRNAs examined, 79 miRNAs (24%) responded to the hyperandrogenic condition and interestingly, 80% of which were upregulated compared to the control group supporting the notion that hyperandrogenic condition down-regulates androgen receptors in the granulosa cells [35] which could be mediated by these upregulated miRNAs (rno-miR-379*, rno-let-7d, rno-miR-24, rno-miR-673, rno-miR-26b, rno-miR-335, rno-miR-382*, rno-miR-412, rno-miR-99a*, rno-miR-543, rno-miR-674-3p, rno-miR-409-3p). [score:9]
A list of differentially expressed miRNAs (Fold change ≥ 2 and their corresponding P value) is presented in Figure  4. Beside this group, miRNAs which were also highly abundant in DHT -treated ovaries are rno-miR-221, rno-miR-222, rno-miR-25, rno-miR-26b, rno-miR-379*, rno-let-7d, rno-miR-24, rno-miR-673, rno-miR-26b, rno-miR-335, rno-miR-382*, rno-miR-412, rno-miR-99a*, rno-miR-543, rno-miR-674-3p, rno-miR-409-3p. [score:3]
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5
[+] score: 11
miRNA expression profiling of lung tissues demonstrated differential expression of seven miRNAs, with downregulation of miR-344a-3p (−2.36-fold change) and upregulation of miR-103 (4.04-fold change), miR-22 (2.72-fold change), miR-30b-5p (1.51-fold change), miR-347 (1.95-fold change), miR-382 (2.82-fold change), and miR-3573-3p (3.32-fold change) (Figures 3A,B). [score:11]
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[+] score: 10
This connectivity diagram showed the multitude of regulatory interactions between these seven miRNAs and their three target mRNAs because miR-382 is also FGF2-regulated, targets c-Maf, resides at the rat chromosome 6 gene cluster of 61 miRNAs, and was included in Figure 7A. [score:7]
We predict that several important regulatory genes of lens fiber cell differentiation, including c-Maf, Kdm5b/Jarid1b, Med1/PBP, Nfat5/OREBP, and N-Myc, are connected by multiple shared miRNAs, with four of them, including miR-381, miR-495, miR-382, and miR-543, encoded by a miRNA cluster on rat chromosome 6, a syntenic region with mouse chromosome 12, and human 14q32.2 imprinted regions. [score:2]
The miR-381, miR-495, miR-543, and miR-382 form a miRNA-gene cluster on rat chromosome 6q32. [score:1]
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7
[+] score: 10
Exemplification showed that miR-150 regulated cell proliferation by targeting VEGF [25], besides miR-382 negatively regulated PTEN expression and increased Akt phosphorylation during LR [35]. [score:7]
From the co -expression network, the obvious conclusion was that miR-150 was related with nine circRNAs, and miR-382 was related with 22 circRNAs. [score:3]
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8
[+] score: 6
Some miRNAs which have been previously reported to be involved in brain disorders and drug abuse, including miR-133b, miR-134, miR-181c, miR-191, miR-22, miR-26b, miR-382, miR-409-3p and miR-504, were found to be changed in their expression following repeated cocaine exposure and subsequent abstinence from cocaine treatment. [score:3]
Twelve miRNAs (miR-135a, miR-190, miR-22, miR-347, miR-376*, miR-380*, miR-382, miR-383, miR-702-3p, miR-708, miR-873, and miR-99b*) were regulated only in CCE rats (p < 0.05 vs. [score:2]
For instance, chronic cocaine exposure also changes the levels of miR-382 and miR-409-3p in nucleus accumbens [12]. [score:1]
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9
[+] score: 6
Treatment with triptolide enhanced expression of five miRNAs (rno-miR-146b-5p, rno-miR-20b-5p, rno-miR-142-3p, rno-miR-223-3p, and rno-miR-21-5p), while that of five other miRNAs (rno-miR-668, rno-miR-203-3p, rno-miR-382-5p, rno-miR-344b-3p, and rno-miR-30b-3p) was significantly downregulated (Tables 3 and 4, and Figure 8). [score:6]
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10
[+] score: 1
Several miRNAs, such as the miR-29 family, miR-382 and miR-21, have been shown to be relevant to renal injury and repair [25], [47]– [49]. [score:1]
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