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37 publications mentioning rno-mir-320

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-320. 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: 411
Figure 2 A. myocardial cells transfected with miR-320 inhibitors overexpression; B. myocardial cells transfected with miR-320 mimics; C. myocardial cells transfected with ad-IGF-1. A. myocardial cells transfected with miR-320 inhibitors overexpression; B. myocardial cells transfected with miR-320 mimics; C. myocardial cells transfected with ad-IGF-1. In vivo experiments showed that, compared with the sham group, miR-320 expression increased in the I/R, I/R + NC and I/R + ad-IGF-1 groups, suggesting increased miR-320 expression after I/R treatment (all P < 0.05). [score:12]
The cells were divided into eight groups: 1) Control group: cells were cultivated in normoxic condition; 2) H/R group: cells were subjected to 10 hours of hypoxia and 2 h of reoxygenation; 3) H/R + negative control (NC) group: cells were transfected with NC (an empty vector) and subjected to 10 h of hypoxia and 2 h of reoxygenation; 4) H/R + miR-320 inhibitor group: cells were transfected with 50 nM miR-320 inhibitors and subjected to 10 h of hypoxia and 2 h of reoxygenation; 5) HR + ad-IGF-1 group: cells were transfected with ad-IGF-1 and subjected to 10 h of hypoxia and 2 h of reoxygenation; 6) H/R + miR-320 mimics+ ad-IGF-1 group: cells were transfected with ad-IGF-1 and subjected to 10 h of hypoxia and 2 h of reoxygenation; 7) Control + miR-320 inhibitors group: cells were cultured under normal oxygen condition after transfected with miR-320 inhibitors lentivirus; and 8) Control + miR-320 mimics + ad-IGF-1 group: cells were cultured under normal oxygen condition after transfected with miR-320 inhibitors and ad-IGF-1 lentivirus. [score:11]
Both in vivo and in vitro experiments show that I/R ands can lower the expression of miR-320 while elevating the expression of IGF-1 mRNA and protein levels, further suggesting that miR-320 inhibits the expression of IGF-1 mRNA and protein levels. [score:9]
Both in vivo and in vitro experiments showed that cell apoptosis rates increase after I/R treatment and that inhibition of miR-320 can target IGF-1, therebydecreasing myocardial cell apoptosis as well as the expression of pro-apoptosis factors Bax and Caspase-3, while increasing the expression of anti-apoptosis factor Bcl-2. Figure 7 A–B. [score:9]
Both in vivo and in vitro experiments showed that cell apoptosis rates increase after I/R treatment and that inhibition of miR-320 can target IGF-1, therebydecreasing myocardial cell apoptosis as well as the expression of pro-apoptosis factors Bax and Caspase-3, while increasing the expression of anti-apoptosis factor Bcl-2. Figure 7 A–B. [score:9]
Furthermore, a recent study has suggested that miR- 320 could inhibit tumor development and growth through targeting IGF-1, and miR-320 might act as a new effective target for the treatment of cancer [19]. [score:8]
MiR-320 mimics increased miR-320 expression in the H/R + miR-320 mimics + ad-IGF-1 group, while miR-320 inhibitors reduced miR-320 expression in the H/R + miR-320 inhibitor group, compared with the H/R, H/R + NC and H/R + ad-IGF-1 groups (all P < 0.05). [score:8]
Figure 2 A. myocardial cells transfected with miR-320 inhibitors overexpression; B. myocardial cells transfected with miR-320 mimics; C. myocardial cells transfected with ad-IGF-1. In vivo experiments showed that, compared with the sham group, miR-320 expression increased in the I/R, I/R + NC and I/R + ad-IGF-1 groups, suggesting increased miR-320 expression after I/R treatment (all P < 0.05). [score:8]
In addition, overexpression of miR-320 resulted in the inhibition of cell proliferation, invasion, migration, and tumorigenesis by targeting IGF-1, which further regulated the signaling pathways downstream, such as phosphoInositide-3 kinase/ serine-threonine kinases (PI3K/AKT) and Mitogen-Activated Protein Kinase/ extracellular-response kinase (MAPK/ERK) [18]. [score:8]
MiR-320 inhibition thus down-regulates the ASK1-JNK/p38 signaling pathway, thereby inhibiting apoptosis. [score:7]
In comparison with the I/R, I/R + NC and I/R + miR-320 mimics + ad-IGF-1 groups, Bcl-2 expression increased and Bax and Caspase-3 expressions decreased in the I/R + miR-320 inhibitor and I/R + ad-IGF-1 groups (all P < 0.05). [score:7]
In addition, our cardiac function study showed that LVEF and LVFS increased while LVESD and LVEDd decreased in the I/R + miR-320 inhibitor group, suggesting inhibition of miR-320 may target IGF-1 to improve cardiac function after reperfusion. [score:7]
Bcl-2 expression was higher while Bax and Caspase-3 expressions were lower in the H/R + miR-320 inhibitor and H/R + ad-IGF-1 groups (all P < 0.05) than in the H/R, H/R + NC and H/R + miR-320 mimics + ad-IGF-1 groups. [score:7]
Figure 2 A. myocardial cells transfected with miR-320 inhibitors overexpression; B. myocardial cells transfected with miR-320 mimics; C. myocardial cells transfected with ad-IGF-1. A. MiR-320 binding sites in the 3′UTR region of IGF-1 gene detected by TargetScan. [score:7]
Our results show that inhibition of miR-320 using a miR-320 inhibitor protects against myocardial I/R injury specifically by suppressing pro-apoptotic pathways and increasing the activation of anti-apoptotic signals. [score:7]
This suggests upregulation of miR-320 in myocardial microvascular endothelial cells may impair angiogenesis by dysregulating expression of IGF-1 protein and mRNA [16]. [score:7]
Our results suggest that inhibition of miR-320 might promote IGF-1 expression and inhibition of the ASK1-JNK/p38 signaling pathway while reducing myocardial cell apoptosis. [score:7]
Bcl-2 expression significantly increased and Bax and Caspase-3 expressions decreased in sham + miR-320 inhibitor group when compared with sham group and sham + miR-320 mimics + ad-IGF-1 group (all P < 0.05), while there was no statistical significance between sham group and sham + miR-320 mimics + ad-IGF-1 group (P > 0.05). [score:6]
Compared with control group and control + miR-320 inhibitor group, IGF-1 mRNA and protein expressions, IGF-1R and p-IGF-1R levels significantly increased in control + miR-320 inhibitor group (all P < 0.05), while no significant difference was found between control group and control + miR-320 mimics+ ad-IGF-1 group (P > 0.05) (Figure 4B–4D). [score:6]
Bcl-2 expression significantly increased and Bax and Caspase-3 expressions decreased in control + miR-320 inhibitor group when compared with control group and control + miR-320 mimics + ad-IGF-1 group (all P < 0.05), while there was no statistical significance between control group and control + miR-320 mimics + ad-IGF-1 group (P > 0.05). [score:6]
miR-320 inhibitors lentivirus, miR-320 mimics lentivirus and ad-IGF-1 recombinant adenovirus marked by green fluorescent protein (GFP) that transfected with myocardial tissues of rats were used to observe the expressions of GFP by fluorescence microscopy to determine the transfection efficiency. [score:5]
4) I/R + miR-320 inhibitors group: seven days after the rats received intramyocardial injection of lentivirus carrying miR-320 inhibitors, I/R was induced as above. [score:5]
MiR-320 inhibition also decreased ISW and ISW/AARW confirming that miR-320 inhibitors reduce infarct and thereby protect cardiac function. [score:5]
In sum, miR-320 expression worsens myocardial I/R injury, while its inhibition protects against myocardial apoptosis. [score:5]
In comparison with I/R, I/R + NC, and I/R + miR-320 mimics + ad-IGF-1 groups, IGF-1 mRNA and protein expressions and p-IGF-1R levels were markedly increased in the I/R + miR-320 inhibitor group and the I/R + ad-IGF-1 group (all P < 0.05). [score:5]
Our results confirm that miR-320 directly binds to the 3′-UTR region of IGF-1 to negatively regulate IGF-1 expression. [score:5]
These results suggest that inhibition of miR-320 may target IGF-1 to improve the cardiac function after reperfusion. [score:5]
Compared with the sham group, IGF-1 mRNA and protein expressions, IGF-1R and p-IGF-1R levels were downregulated in the I/R treated groups (all P < 0.05), no significant difference was found among I/R group, I/R + NC group, and I/R + miR-320 mimics + ad-IGF-1 group. [score:5]
8) Sham + miR-320 mimics+ ad-IGF-1 group: suture line was placed under the LAD, the coronary artery was not ligated, and the rats received intramyocardial injection of lentivirus carrying miR-320 inhibitors and ad-IGF-1. MiR-320 mimics synthesized by chemical methods stimulated endogenous miR-320 expression in vivo and enhanced endogenous miR-320 function. [score:5]
These results indicate that inhibition of miR-320 may target IGF-1 to improve the hemodynamic index disorder. [score:5]
7) Sham + miR-320 inhibitors group: suture line was placed under the LAD, the coronary artery was not ligated, and the rats received intramyocardial injection of lentivirus carrying miR-320 inhibitors. [score:5]
ASK1-JNK/p38 signaling pathways were activated by I/R and but were suppressed by inhibition of miR-320. [score:5]
These results suggest that miR-320 binds to IGF-1 3′-UTR and inhibits IGF-1 expression. [score:5]
MiR-320 inhibitors are chemically modified to inhibit miR-320. [score:5]
Based on the predicted target binding site of rno-miR-320 and the IGF-1 gene, site-directed mutagenesis was employed to abolish the biding site and this mutant was used as a control. [score:4]
Figure 1MiR-320 targets IGF-1 gene A. MiR-320 binding sites in the 3′UTR region of IGF-1 gene detected by TargetScan. [score:4]
MiR-320 inhibition reduces myocardial I/R injury in mice, and its overexpression increases cardiomyocyte apoptosis and death. [score:4]
MiR-320 inhibition suppresses apoptosis effect mainly via the IGF-1 pathway, affecting the levels of anti-apoptotic Bcl-2 and pro-apoptotic Bax and caspase-3, and inactivating the ASK1-JNK/p38 signaling pathways. [score:4]
MiR-320 binds IGF-1 mRNA and inhibits IGF-1 expression. [score:4]
MiR-320 inhibition decreased the rate of cardiomyocyte apoptosis in vivo and in vitro by increasing Bcl-2 expression and decreasing Bax and Caspase-3 levels. [score:4]
Note: p-ASK1, phosphorylated-apoptosis signal -regulating kinase 1; p-JNK, phosphorylated-c-Jun N-terminal kinase; H/R, hypoxia/reoxygenation; NC, negative control; IGF-1, Insulin-like growth factor 1. We found miR-320 binding sites in the 3′UTR of IGF-1 using thebioinformatics prediction software TargetScan (Figure 1A). [score:4]
Compared with sham group and sham+ miR-320 mimics+ ad-IGF-1 group, IGF-1 mRNA and protein expressions, IGF-1R and p-IGF-1R levels significantly increased in sham + miR-320 inhibitor group (all P < 0.05), while no significant difference was found between sham group and sham + miR-320 mimics + ad-IGF-1 group (P > 0.05) (Figure 3B–3D). [score:4]
However, there was no significant difference in miR-320 expression among the H/R, H/R + NC and H/R + ad-IGF-1 groups (P > 0.05). [score:3]
The effect of miR-320 expression on myocardial cell apoptosis after I/R treatment is shown in Figure 6A–6B. [score:3]
Figure 5s during I/R in the sham, I/R, IR + NC, I/R + miR-320 mimics + ad-IGF-1, I/R + miR-320 inhibitor and I/R + ad-IGF-1 groups. [score:3]
We found miR-320 binding sites in the 3′UTR of IGF-1 using thebioinformatics prediction software TargetScan (Figure 1A). [score:3]
B. Dual-luciferase reporter gene system showing miR-320 targeting IGF-1 gene. [score:3]
This suggests miR-320 may represent a valuable tool and potential therapeutic target for protection against I/R induced cardiac injury. [score:3]
In comparison with the control group, IGF-1 mRNA and protein levels were decreased in other H/R treated groups (all P < 0.05), while there was no significant difference in IGF-1 expression among the H/R, H/R + NC and HR + miR-320 mimics + ad-IGF-1 groups (all P > 0.05). [score:3]
Note: I/R, ischemia/reperfusion; NC, negative control; IGF-1, insulin-like growth factor 1. s during I/R in the sham, I/R, IR + NC, I/R + miR-320 mimics + ad-IGF-1, I/R + miR-320 inhibitor and I/R + ad-IGF-1 groups. [score:3]
In order to verify whether this 3′UTR region of IGF-1 is indeed targeted by miR-320, wild-type (WT) and mutant reporters were constructed with GV126-IGF-1 3′-UTR. [score:3]
The transfection efficiencies of miR-320 inhibitors lentivirus, miR-320 mimics lentivirus and ad-IGF-1 recombinant adenovirus were observed for further experiment. [score:3]
As expected, co-transfection of miR-320 mimics and recombinant mutant GV126-IGF-1 3′-UTR, co-transfection of miR-320 inhibitors and recombinant mutant GV126-IGF-1 3′-UTR, and co-transfection of miR-320 negative control and recombinant vectors showed no luciferase activity (all P > 0.05, Figure 1B). [score:3]
And there was no significant difference between I/R + ad-IGF-1 group and I/R + miR-320 inhibitor group (all P > 0.05). [score:3]
Although the mechanistic link between miR-320 and the ASK1-JNK/p38 signaling pathway requires further examination, we hypothesize that IGF-1 increases ASK1 expression to modulate the ASK1-JNK/p38 signaling pathway. [score:3]
Apoptosis rates were lower in the H/R + miR-320 inhibitor (28.45 ± 2.69%) and HR + ad-IGF-1 (27.18 ± 2.17%) groups (all P < 0.05) than in the H/R, H/R + NC and H/R + miR-320 mimics + ad-IGF-1 groups. [score:3]
In comparison with the I/R, I/R + NC and I/R + miR-320 mimics + ad-IGF-1 groups, apoptosis rates significantly decreased in the I/R + miR-320 inhibitor and I/R + ad-IGF-1 groups (25.49 ±1.69 % and 26.62 ± 1.22 %, respectively) (all P < 0.05). [score:3]
MiR-320 mimics sequence: 5′-AAAAGCUGGGUUGAGAGGGCGA-′3, miR-320 inhibitors sequence: 5′-UCGCCCUCU CAACCCAGCUUUU-′3 (Shanghai GenePharma Co. [score:3]
MiR-320 inhibitor lentivirus marked by GFP, miR-320 mimic lentivirus, empty viral vectors and ad-IGF-1 recombinant adenovirus (titer: 4.0×10 [8]pfu/ml) were purchased from Shanghai genechem Gene Technology Co. [score:3]
In comparison with the H/R, H/R + NC and H/R + miR-320 mimics + ad-IGF-1 groups, p-ASK1, p-JNK and p-p38 levels were lower in the H/R + miR-320 inhibitor and H/R + ad-IGF-1 groups (all P < 0.05) (Figure 9). [score:3]
On the other hand, these indexes are sharply reduced by I/R treatment, which highlight the positive effects of miR-320 inhibition on the recovery of cardiac function. [score:3]
BW, body weight; LVW, left ventricle weight; AARW, area at risk weight; ISW, infarct size weight; I/R, ischemia/reperfusion; NC, negative control; miR-320, microRNA-320; IGF-1, insulin like growth factor-1. In order to further test whether inhibition of miR-320 can target IGF-1 to reduce myocardial cell apoptosis, we measured apoptosis rates as well as levels of apoptosis-related factors, Bcl-2, Bax and Caspase-3 in rat myocardial tissues and cells. [score:3]
Interestingly, miR-320 inhibitor decreases activation of p-ASK1, p-JNK and p-p38. [score:3]
MiR-320 mimics, miR-320 inhibitors and a negative control (NC) were respectively co -transfected with the luciferase reporter vector into HEK293 cells. [score:3]
Note: miR-320, microRNA-320; IGF-1, Insulin-like growth factor 1; UTR, untranslated region; wt, wild type; mut, mutant type. [score:3]
These results imply that miR-320 might target IGF-1 to lower MI size. [score:3]
Real time-PCR detecting miR-320 and IGF-1 mRNA expressions. [score:3]
The absolute values of SBP, DBP, MAP and ± dp/dtmax in sham + miR-320 inhibitor group were significantly higher than those in the same time point of sham group and sham + miR-320 mimics + ad-IGF-1 group (P < 0.01), while no significant difference was found in each index of different time points between sham group and sham+ miR-320 mimics+ ad-IGF-1 group (P > 0.05) (Figure 5). [score:3]
We found that miR-320 inhibitors increase the absolute values for SBP, DBP, MAP and ± dp/dtmax. [score:3]
However, there was no difference in miR-320 expression between the I/R, I/R + NC and I/R + ad-IGF-1 groups (all P > 0.05). [score:3]
In a previous study, we demonstrated that miR-320 inhibition using antagomir-320 protects the left ventricle from remo deling after I/R injury [15]. [score:3]
org were employed to predict possible targets of rno-miR-320. [score:3]
Conversely, co-transfection of miR-320 inhibitors and recombinant WT GV126-IGF-1 3′-UTR increased luciferase activity (P < 0.05). [score:3]
Real time-PCR detecting miR-320 and IGF-1 mRNA expressions. [score:3]
Particularly, miR-320 was reported to have the potential to target multiple angiogenesis-related genes, such as Flk-1, VEGF-c, IGF-1, IGF-1R and FGFs [16]. [score:3]
Our results show that IGF-1 mRNA and protein levels correlate negatively with miR-320 levels, suggesting that IGF-1 mRNA might be an important miR-320 target in vivo. [score:3]
We also tested for the effects of miR-320 expression on several hemodynamic indexes, myocardial infarct (MI) size and cardiomyocyte apoptosis. [score:3]
Compared with sham group, miR-320 levels significantly decreased in sham + miR-320 inhibitor group while increased remarkably in sham + miR-320 mimics + ad-IGF-1 group (both P < 0.05) (Figure 3A). [score:2]
MiR-320 and IGF-1 expressions in myocardial tissue and cells. [score:2]
MiR-320 and IGF-1 mRNA and protein expressions in myocardial tissue. [score:2]
MiR-320 targets IGF-1 gene. [score:2]
Compared with the I/R, I/R + NC and I/R + ad-IGF-1 groups, miR-320 levels increased remarkably in the I/R + miR-320 mimics + ad-IGF-1 group, but decreased in the I/R + miR-320 inhibitor group (all P < 0.05). [score:2]
6) I/R + miR-320 mimics + ad-IGF-1 group: miR-320 mimics and ad-IGF-1 recombinant adenovirus were directly injected to the myocardium, and 7 days later LAD was ligated reversibly. [score:2]
p-ASK1, p-JNK and p-p38 levels significantly decreased in sham + miR-320 inhibitor group when compared with sham group and sham + miR-320 mimics + ad-IGF-1 group (all P < 0.05), while there was no statistical significance between sham group and sham + miR-320 mimics + ad-IGF-1 group (P > 0.05) (Figure 8). [score:2]
In vitro experiments showed that, compared with the control group, miR-320 expression increased in H/R -treated groups (all P < 0.05). [score:2]
The absolute values of SBP, DBP, MAP and ± dp/dtmax were higher in the I/R + miR-320 inhibitor and I/R + ad-IGF-1 groups compared with the I/R, I/R + NC and I/R + miR-320 mimics + ad-IGF-1 groups at each time point (all P < 0.01). [score:2]
p-ASK1, p-JNK and p-p38 levels significantly decreased in control + miR-320 inhibitor group when compared with control group and control + miR-320 mimics + ad-IGF-1 group (all P < 0.05), while there was no statistical significance between control group and control + miR-320 mimics + ad-IGF-1 group (P > 0.05). [score:2]
LVEF and LVFS remarkably increased while LVESD and LVEDd decreased significantly in sham + miR-320 inhibitor group when compared with sham group and sham + miR-320 mimics + ad-IGF-1 group (all P < 0.05), while there was no statistical significance between sham group and sham + miR-320 mimics + ad-IGF-1 group (P > 0.05). [score:2]
Our results showed that, compared with other groups, co-transfection of miR-320 mimics and recombinant WT GV126-IGF-1 3′-UTR inhibited luciferase activity. [score:2]
Compared with the I/R, I/R + NC and I/R + miR-320 mimics + ad-IGF-1 groups, p-ASK1, p-JNK and p-p38 levels decreased in the I/R + miR-320 inhibitor and I/R + ad-IGF-1 groups (all P < 0.05). [score:2]
MiR-320 and IGF-1 mRNA and protein expressions in rat myocardial cells. [score:2]
However, there was no statistically significant difference among the I/R, I/R + NC and I/R + miR-320 mimics + ad-IGF-1 groups (all P > 0.05); and compared with the I/R, I/R + NC and I/R + miR-320 mimics+ ad-IGF-1 groups, LVEF and LVFS increased while LVESD and LVEDd decreased in the I/R + miR-320 inhibitor and I/R + ad-IGF-1 groups (all P < 0.05). [score:2]
Compared with control group, miR-320 levels significantly decreased in control + miR-320 inhibitor group while increased remarkably in control + miR-320 mimics + ad-IGF-1 group (both P < 0.05) (Figure 4A). [score:2]
Compared with the H/R, H/R + NC and HR + miR-320 mimics + ad-IGF-1 groups, IGF-1 mRNA and protein levels were increased in the H/R + miR-320 inhibitor group and the HR + ad-IGF-1 group (all P < 0.05). [score:2]
The infarct size weight (ISW) and ISW/AARW showed no differences among the I/R, I/R + NC and I/R + miR-320 mimics + ad-IGF-1 groups (P > 0.05), but markedly decreased in the I/R + miR-320 inhibitor group and the I/R + ad-IGF-1 group compared with the I/R, I/R + NC and I/R + miR-320 mimics + ad-IGF-1 groups (all P < 0.05) (Table 2). [score:2]
However, the cellular pathways stimulated by miR-320 in myocardial I/R injury are currently unknown [11]. [score:1]
Finally, we conducted in vitro hypoxia-reoxygenation (H/R) experiments using rat cardiomyocytes to simulate I/R and to verify the actions of miR-320 in myocardial I/R injury. [score:1]
Note: miR-320, microRNA-320; IGF-1, Insulin-like growth factor 1; PCR, polymerase chain reaction. [score:1]
LVEF, left ventricular ejection fraction; LVFS, left ventricular fraction shortening; LVESD, left ventricular end systolic diameter; LVEDd, left ventricular end diastolic diameter; I/R, ischemia/reperfusion; NC, negative control; miR-320, microRNA-320; IGF-1, insulin like growth factor-1. A–B. [score:1]
Note: Bcl-2, B-cell lymphoma 2; H/R, hypoxia/reoxygenation; NC, negative control; IGF-1, Insulin-like growth factor 1. To test whether miR-320 targets IGF-1 to activate the ASK1-JNK/p38 signaling pathway and increase myocardial cell apoptosis, we measured cell apoptosis downstream of the ASK1-JNK/p38 signaling pathway. [score:1]
LVEF, left ventricular ejection fraction; LVFS, left ventricular fraction shortening; LVESD, left ventricular end systolic diameter; LVEDd, left ventricular end diastolic diameter; I/R, ischemia/reperfusion; NC, negative control; miR-320, microRNA-320; IGF-1, insulin like growth factor-1. The body weight (BW), left ventricle weight (LVW), area at risk weight (AARW) and AARW/LVW showed no differences among the I/R treated groups (all P > 0.05). [score:1]
A myocardial I/R injury mo del was successfully induced in rats by occlusion/reperfusion of the left anterior descending coronary artery, and the rats were intramyocardially injected with lentiviral vector encoding miR-320 to study its actions within cardiomyocytes. [score:1]
However, no significant difference in hemodynamic indexes was observed among the I/R, I/R + NC and I/R + miR-320 mimics + ad-IGF-1 groups at any time point (all P > 0.05). [score:1]
Reaction conditions (miR-320) were: initial denaturation at 95°C for 10 min, and 40 cycles of denaturation at 95°C for 15 s and annealing at 60°C for 1 min. [score:1]
qRT-PCR to detect miR-320 and IGF-1 mRNA. [score:1]
The apoptosis rate in the H/R, H/R + NC and H/R + miR-320 mimics + ad-IGF-1 groups showed no significant differences (47.45 ± 2.54% vs. [score:1]
However, no significant differences in p-ASK1, p-JNK and p-p38 levels were observed among the H/R, H/R + NC and H/R + miR-320 mimics + ad-IGF-1 groups (all P > 0.05). [score:1]
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[+] score: 152
Other miRNAs from this paper: mmu-mir-320
Dysregulated expression of the miR-320 in many tumor [15, 16] was strongly associated with tumor development, and miR-320 expression level was down-regulated greater than two fold in primary breast cancer (BC) [15]. [score:10]
MiR-320 expression level was down-regulated in primary breast cancer (BC) [15], and inhibited HL-60 cell proliferation by targets transferrin receptor 1 (CD71) [16]. [score:9]
After implantation was activated by estrogen treatment and the embryos had implanted, there was weak miR-320 expression in the stroma, glandular and luminal epithelia (Figure 3 B c), suggesting that down-regulation of miR-320 expression was dependent upon the presence of viable implanting blastocysts. [score:8]
This indicated that artificial decidualization promoted the expression of miR-320 and further emphasize the importance of decidualization in regulating the dynamics of miR-320 expression in the uterus during the window of implantation. [score:6]
In order to test the effect of steroid hormones on the miR-320 expression under physiological condition, Northern blot was performed to examine whether the miR-320 expression was regulated by steroid hormones. [score:6]
Delayed implantation inhibited the expression of miR-320. [score:5]
The expression of miR-320 is decreased on g. d. 5, but its expression was increased by progesterone under physiological condition. [score:5]
These results imply that the action of progesterone on miR-320 expression might inhibit the excess invasion of cells from the uterus and trophectoderm. [score:5]
These results implied that the low expression of miR-320 may be benefit to formation of endometrial receptivity under pregnant condition and the high expression of miR-320 may be in favor of the maintenance of female endocrine homeostasis. [score:5]
The in situ results were from interimplantation uterine regions on g. d. 6. The above-mentioned observations suggested that the presence of blastocysts may reduce the expression of miR-320 in the uterine luminal epithelia and stroma and decidualization may induce the expression of miR-320 in pregnant rats. [score:5]
However, treatment with progesterone significantly increased miR-320 expression (P < 0.01) and estradiol-17β did not visibly affect the expression level of miR-320. [score:5]
Schaar DG Medina DJ Moore DF Strair RK Ting Y MiR-320 targets transferrin receptor 1 (CD71) and inhibits cell proliferationExp. [score:4]
In addition, this expression of miR-320 was regulated by progesterone. [score:4]
To test whether miR-320 expression was regulated by decidualization, a mo del of experimentally induced decidualization was used for Northern blot and in situ hybridization analyses. [score:4]
The expression level of miR-320 in the decidualized uterus was evidently higher than in the nonstimulated uterus on day 7 of pseudopregnancy (Figure 4 A). [score:3]
These results suggested that the miR-320 expression is not dependent upon the presence of embryos in pregnant rats. [score:3]
A low level of miR-320 expression was detected in the ovariectomized rat uterus. [score:3]
Experimentally induced decidualization increases the expression of miR-320. [score:3]
To test whether the miR-320 expression was dependent upon embryo implantation status, a delayed implantation mo del was used for Northern blot and in situ hybridization analyses. [score:3]
We studied the effect of pseudopregnancy, artificial decidualization and activation of delayed implantation on the expression of miR-320. [score:3]
The expression level of mir-320 detected by Northern blot was not significantly different in uterus during days 3–7 of pseudopregnancy. [score:3]
In addition, we also tested the effect of steroid hormones on miR-320 expression. [score:3]
Progesterone enhances the miR-320 expression. [score:3]
Here, we report the expression pattern of miR-320 in the uterus during embryo implantation in the rat. [score:3]
Differential expression of miR-320 in the rat uterus during the peri-implantation period. [score:3]
The miR-320 expression was slightly increased by combination of both (Figure 5). [score:3]
Pseudopregnancy did not change the expression of miR-320. [score:3]
The expression level of miR-320 is higher during g. d. 3–4 than g. d. 5–7 in the stroma. [score:3]
All these facts indicated that progesterone can promote miR-320 expression under physiological condition. [score:3]
showed that the expression level of miR-320 was lower on g. d. 5 in rats than g. d. 3 and g. d. 4 (p < 0.05), and restored gradually from g. d. 6, and was higher on g. d. 8 and g. d. 9 than g. d. 5 (p < 0.05) (Figure 1 A). [score:3]
The results obtained from our mo dels of pseudopregnancy, artificial decidualization and delayed implantation imply an important role for implanting blastocysts and decidualization in the temporal and spatial changes of miR-320 expression in the uterus during the window of implantation. [score:3]
To test the effects of steroid hormones on miR-320 expression, rats were treated with hormones starting 2 weeks after they were ovariectomized. [score:3]
To see whether the miR-320 expression was dependent upon the presence of embryos, uterine tissues were subjected to Northern blot and in situ hybridization analysis (Figure 2 A). [score:3]
This implied that miR-320 may play an important role in the development of cancer. [score:2]
Northern blot showed a high level of miR-320 in the uterus under delayed implantation conditions, but it decreased significantly after implantation was activated with estrogen treatment (P < 0.05; Figure 3 A). [score:1]
The human miR-320 sequence was originally cloned from the normal mucosa-derived population of human[12] and rat miR-320 sequence was firstly found from large-scale cloning studies [14]. [score:1]
I n situ hybridization showed that the miR-320 signal was mainly found in uterine glandular and luminal epithelia during days 3–7 of pseudopregnancy (Figure 2 B). [score:1]
To study the role of miR-320 in embryo implantation, we first examined its temporal and spatial distribution in the uterus during the peri-implantation period in rat. [score:1]
Mouse mir-320 was predicted [11] based on homology to a cloned human miRNA (MI0000542) [12] and cloned from mouse oocytes and testes [13]. [score:1]
In situ hybridization of miR-320 with DIG-labeled LNA probes. [score:1]
On g. d. 5, the miR-320 signal mainly appeared in the glandular epithelia and weak in the luminal epithelia and stroma (Figure 1 B c). [score:1]
In conclusion, we found that the miRNA miR-320 could be detected differentially in the rat uterus during the peri-implantation period. [score:1]
Collectively, these findings will help us gain a better understanding of the role of mir-320 during pregnancy and provide a foundation for futher experimental studies on mechanisms mechanisms associated with the onset of uterine receptivity and embryo implantation. [score:1]
After acetylation with 0.25% acetic anhydride in 0.1 M triethanolamine (pH 8.0) for 10 min, sections were prehybridized with hybridization buffer (Roche, Mannheim, Germany) at 40 °C for 2h and then hybridized with digoxigenin (DIG)-labeled LNA-miR-320 probe (LNA-miR-320 sequence: 5′–DIG–ttCgcCctCtCaAcCcAgCtttt–3′) at 40 °C overnight. [score:1]
The in situ hybridization results showed that the miR-320 was mainly located in the glandular, luminal epithelia and stroma on g. d. 3 and g. d. 4 (Figure 1 B a and b). [score:1]
A miR-320 signal was found in the deciduas, glandular and luminal epithelia on g. d. 6 (Figure 1 B d) and was strengthened in deciduas from g. d. 7 (Figure 1 B e). [score:1]
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3
[+] score: 115
Over -expression of miR-320 enhances cell death and apoptosis in cultured adult rat cardiomyocytes on simulated I/R injury; thus, down-regulation of miR-320 expression may be involved in the protection against cardiac hypertrophic remo deling, but the molecular mechanisms are still not completely understood [25]. [score:8]
In addition, we found that the degree of fibrosis remo deling in the I/R + antagomir-320 group was apparently lower than that in the I/R group at each time point, implying that the downregulation of the expression of miR-320 may inhibit the formation of myocardial fibrosis after myocardial I/R. [score:8]
Subsequently, miR-320 expression is up-regulated in patients with failing hearts in contrast to the healthy controls and is associated with potential cardiovascular target genes [23]. [score:8]
The reason why miR-320 was associated with the degree of myocardial damage may be that over -expression of miR-320 may downregulate the heat-shock protein 20 (Hsp20), which may protect the heart against myocardial I/R injury, while the decreased expression of miR-320 may reduce infarct size [15, 22]. [score:8]
Our study further confirmed that the cardiac-specific expression of miR-320 has an increased expression in mouse mo dels with myocardial I/R injury and a decreased miR-320 expression level, which may promote the improvement of heart function along with the treatment of antagomir-320. [score:7]
In this study, the qRT-PCR results also indicated that the miR-320 expression levels in the I/R group were apparently up-regulated when compared with those in the sham group, suggesting that the miR-320 expression levels were closely associated with the myocardial I/R injury, and the increased miR-320 levels may have acted as a risk factor for myocardial I/R injury. [score:7]
It has been revealed that miR-320 expression in human left ventricular samples was significantly altered in the heart disease group and the control group, showing evidence of the over -expression of miR-320 in ischemic cardiomyopathy and aortic stenosis [24]. [score:7]
To summarize, our study results support the view that the expression of miR-320 might be up-regulated in the rat mo del of myocardial I/R injury, and miR-320 might contribute to the prevention of left ventricular remo deling after myocardial I/R injury. [score:6]
An increased expression level of miR-320 may lead to cell apoptosis or death and may increase infarct size after I/R injury, while the knockdown of miR-320 expression may have obviously protective effects on cells [22, 50]. [score:6]
Furthermore, decreased endogenous miR-320 expression may reduce cardiomyocyte apoptosis when induced by simulated I/R, whereas over -expression of miR-320 increased sensitivity to I/R-triggered cell death [22]. [score:5]
Schaar D. G. Medina D. J. Moore D. F. Strair R. K. Ting Y. miR-320 targets transferrin receptor 1 (CD71) and inhibits cell proliferation Exp. [score:5]
On the other hand, an increased miR-320 expression level has been reported to promote cell apoptosis and to inhibit neoangiogenesis, which may be related to myocardial I/R injury [46]. [score:5]
More specifically, miR-320, a member of the miR family, plays functional roles in the inhibition of cell division, acting in stromal fibroblasts and regulating glycolysis, which may play important roles in the fibrosis development associated with left ventricular remo deling and in the energy metabolism of IHD [20, 21, 22]. [score:5]
Thus, both loss-of-function and gain-of-function studies have suggested that miR-320 expression is a negative regulator of cardio protection against I/R injury [24, 52, 53]. [score:4]
It has been reported that circulating cardio-enriched miRs might be negatively associated with LVEF [45]; hence, we suspected that miR-320 expression may also regulate the changes of cardiac hemodynamics. [score:4]
qRT-PCR was applied to detect the expression of miR-320 in the three groups. [score:3]
ijms-15-17442-t004_Table 4 Table 4 Expression of miR-320 in the myocardial tissue of three groups at five time points. [score:3]
2.5. miR-320 Expression in Myocardial Tissue. [score:3]
These results suggested that the decreased miR-320 expression level may decrease the degree of myocardial damage, reduce the risk of ventricular remo deling after surgery and, then, improve heart function. [score:3]
miR-320 may play an important regulatory role in cell proliferation, cell differentiation and also cell apoptosis [51]. [score:2]
Consequently, decreased miR-320 expression may, in turn, be considered as a possible predictive factor in reducing the risk of left ventricular remo deling risk after myocardial I/R injury and improving cardiac function. [score:2]
Meanwhile, we observed that the expression of miR-320 dramatically decreased in the I/R + antagomir-320 group compared with the I/R group during day 3 to day 30 after surgery (all p < 0.05). [score:2]
These outcomes have suggesting that myocardial I/R may induce myocardial cell apoptosis and that treatment with miR-320 can reduce myocardial cell apoptosis. [score:1]
As previously mentioned, miR-320 seems to play a key role in myocardial I/R injury myocardial infarction, cell angiogenesis, cardiac hypertrophy, myocardial fibrosis and the protection of cardiac function. [score:1]
We also explored whether miR-320 is implicated in the process to preserve cardiac function. [score:1]
The purpose of this study is to investigate the role of miR-320 in myocardial I/R injury and to observe miR-320 expression in left ventricular remo deling after myocardial I/R injury. [score:1]
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4
[+] score: 61
Since the down-regulation of microRNAs may cause the up-regulation of targeted genes, we hypothesized that the presence of IGF-1 triggers the expression of certain genes by down -regulating key microRNAs (miR-1224, miR-125a-3p, miR-214, miR-22, miR-320, miR-708, and miR-93), which in turn enhance NPCs proliferation and survivability. [score:12]
Protein kinase B or Akt, a key protein involved in the activation of PI3K-Akt pathway and is crucial in promoting cell survivability [43], is inhibited by the key microRNAs (miR-22, miR-214, miR-125a-3p, miR-320 and let-7 family) that are down-regulated with the addition of IGF-1. Chen et al. reported that down-regulation of miR-133b significantly overexpressed Akt1 mRNA, which increased T24 bladder cancer cell proliferation and reduced cell apoptosis [44]. [score:11]
However, BMSC-derived NPCs with addition of IGF-1 showed 12 microRNAs which include miR-22, miR-1224, miR-125a-3p, miR-214, miR-320, miR-708 and miR-93 were consistently down-regulated and only miR-496 remained up-regulated compared to Group C from Day 1 to Day 5. The let-7 family (let-7b, let-7c, let-7d, let-7e and let-7i) were constantly down-regulated in both groups. [score:9]
Furthermore, the introduction of IGF-1 triggers the down-regulation of several microRNAs (miR-214, miR-22, miR-320 and miR-708) with their inconsistent differential expression in Group A. The inhibition of miR-214 has been reported to decrease the level of apoptosis in HeLa cells [34]. [score:8]
The genes up-regulated by down-regulation of miR-22 (A); miR-125a-3p (B); let-7 family (C); miR-214 (D); and miR-320 (E) were analyzed using GeneMANIA web tool with default weighting method (i. e., weighting based to maximize connectivity between input genes). [score:7]
MicroRNAs Query Genes miR-22 Myc; Ets1; Tp53; Agt; Esr1; Pten; Akt1 miR-214 Bcl2; Adora1; Myc; Neurod1; Dhcr24; Kras; Fgfr1; Apc; pcgfr1; Prnp; Akt1 miR-125a-3p Bcl2; Egfr; Tp53; Apc; Akt1; Rela miR-320 Bcl2; Adora1; Acvr1; Neurod1; Dhcr24; Tp53; Hmox1; Nol3; Pten; Akt1; Cebpb Let-7 Family Cdkn1a; Tnf; Bcl2; Adora1; Egfr; Myc; Il10; Acvr1; Sycp3; Neurod1; Dhcr24; Cdkn1b; SMAD3; Kras; ras3; Neurod1Birc2; Tp53; Kcnh8; FN1; Fgfr1; Clu; Fas; Pten; Akt1; Rela; Cebpb We assessed the predicted target genes of the down-regulated microRNAs with the KEGG database. [score:6]
Schaar D. G. Medina D. J. Moore D. F. Strair R. K. Ting Y. miR-320 targets transferrin receptor 1 (CD71) and inhibits cell proliferation Exp. [score:5]
Query genes for individual microRNA are listed in Table 5. The major targeted genes by all or four out of five key microRNAs (miR-22, miR-214, miR-125a-3p, miR-320 and let-7 family) included Akt1, Tp53, Pten and Bcl2. [score:3]
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5
[+] score: 40
miR-29a, miR-144, miR-150, miR-192 and miR-320 showed an up-regulation from that of control samples whereas miR-30d, miR-146a and miR-182 showed down-regulation. [score:7]
miR-30d and miR-320 which have been shown to regulate INS and PIK3/Akt signaling [50] exhibited opposite expression in the two disease groups (Table S8). [score:6]
miR-29a and miR-320 that have been previously found to show altered expression in diabetic mo dels [34], [49], [50], also showed a significant up-regulation in the T2D samples in our study. [score:6]
CBL and GLUT4 are potential targets of miR-150, while miR-320 inhibits PI3-K/Akt signaling [50]. [score:5]
miR-30d expression has been strongly associated to insulin gene transcription [49], while miR-320 was reported to affect the AKT signaling pathway [50]. [score:3]
miR-29a, miR-30d, miR-150 and miR-320 are all highly expressed in adipose, skeletal muscle and liver tissues with lower abundance in pancreas. [score:3]
The eight miRNAs (miR-144, miR-146a, miR-150, mR-182, miR-192, miR-29a, miR-30d and miR-320) which were previously identified in the rat study showed similar expression in the patients' blood miRNAs. [score:3]
Clin Exp Pharmacol Physiol Epub ahead of print 51 Wang XH Qian RZ Zhang W Chen SF Jin HM 2009 MicroRNA-320 expression in myocardial microvascular endothelial cells and its relationship with insulin-like growth factor-1 in type 2 diabetic rats. [score:2]
We have also identified eight important miRNAs (miR-144, miR-146a, miR-150, miR-182, miR-192, mir-29a, miR-30d and miR-320) that could participate in the regulation of insulin signaling as well as useful in distinguishing different stages of diabetes progression. [score:2]
Although our results were in conjunction with earlier studies which identified miR-192, miR-29a, miR-320 and miR-30d to be potential key players in the pathogenesis of T2D, we do observe differences in the recent study reported by Zampetaki et al [20]. [score:1]
Association of miR-192 [35], miR-29a [34] and miR-320 [50], [51] in T2D has been reported in previous studies and our study also shows similar results. [score:1]
Predictions: miR-144/ IRS1; miR-146a/ PTPN1; miR-150/ GLUT4 and CBL; miR-182/ FOXO1; miR-192/ INSR; miR-30d/ INS; miR-29a and miR-320/ AKT2. [score:1]
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6
[+] score: 35
As illustrated in Figure 7, miR-27b and miR-7a were up-regulated whereas miR-343-3p and miR-320 were down-regulated by RDX. [score:7]
MiR-27b and miR-320 were up-regulated and down-regulated respectively in our study, but not significantly changed in mouse brain tissue. [score:7]
MiRNAs Target Genes Names Regulation Up Down miR-135a Up KIAA1033, CEP350, ROCK2 miR-320 Down BANP, CALD1, POLE4 miR-98 Up SULF1 miR-129* Down BANP, FAM82A2 miR-27ab Up HMGCR, LITAF, NPTX2 CALD1, C5orf13, KIAA1033 miR-342-3P Down VGF KIAA1033 miR-7a Up SLC38A2 POLE4, SLC35E4, C5orf13 miR-674-5p Up VGFBiological functional analysis revealed that more than half (8) of the overlapped genes are involved in neurological diseases and nervous system function (Table 4). [score:6]
MiRNAs Target Genes Names Regulation Up Down miR-135a Up KIAA1033, CEP350, ROCK2 miR-320 Down BANP, CALD1, POLE4 miR-98 Up SULF1 miR-129* Down BANP, FAM82A2 miR-27ab Up HMGCR, LITAF, NPTX2 CALD1, C5orf13, KIAA1033 miR-342-3P Down VGF KIAA1033 miR-7a Up SLC38A2 POLE4, SLC35E4, C5orf13 miR-674-5p Up VGF Biological functional analysis revealed that more than half (8) of the overlapped genes are involved in neurological diseases and nervous system function (Table 4). [score:6]
The expression of miR-320, miR-129* and miR-342-3p was significantly down-regulated by RDX. [score:6]
MiR-320, rno-miR-129* and their targets were both repressed by RDX. [score:3]
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7
[+] score: 18
In contrast, expressions of mir-21 and mir-320 were significantly downregulated and GS-Rb1 incubation in mo del group could reverse the differences in a certain extent. [score:6]
Our results showed that mir-21 and mir-320 significantly decreased in the H/I injured cardiomyocytes and increased by GS-Rb1 treatment following H/I, which suggested that mir-21 and mir-320 might be the potential microRNA targets of GS-Rb1 to protect cardiomyocytes. [score:3]
The expression level of mir-1, mir-29a, and mir-208 was increased in the H/I group (5.9-, 3.4-, and 9.3-fold versus control, relatively), while that of mir-21 and mir-320 was significantly decreased (0.35- and 0.41-fold versus control, relatively). [score:3]
Overexpression of mir-320 enhanced cardiomyocyte apoptosis and increased extent of apoptosis and infarction size in the hearts. [score:3]
Mir-320 expression was significantly decreased in the hearts on ischemia/reperfusion in vivo and in vitro. [score:2]
Mir-320 has the familiar function with mir-21. [score:1]
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8
[+] score: 17
Song C. L. Liu B. Diao H. Y. Shi Y. F. Zhang J. C. Li Y. X. Liu N. Yu Y. P. Wang G. Wang J. P. Down-regulation of microrna-320 suppresses cardiomyocyte apoptosis and protects against myocardial ischemia and reperfusion injury by targeting IGF-1 Oncotarget 2016 10.18632/oncotarget. [score:11]
miRNA-320, which targets ASK1, suppressed cardiomyocyte apoptosis by down -regulating ASK1/JNK phosphorylation under ischemia/reperfusion injury [33]. [score:6]
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9
[+] score: 16
For these miRNAs, both platforms reported them to be similarly regulated; miR-320 was up regulated while let-7d and miR-203 were down regulated (Tables  1 and 4). [score:4]
Regardless of platform differences, the three miRNAs identified by both platforms, let-7d, miR-203 and miR-320, hold promise as tubular injury biomarkers due to their strong functional associations with cellular process or pathways relevant to renal disease. [score:3]
However, all three miRNAs: let-7d, miR-203, and miR-320 were reliably detected by qRT-PCR in every sample with low mean C [t] values (miR-let-7d: 27.52 ± 0.77; miR-203: 24.66 ± 0.3; miR-320: 24.69 ± 1.1) which suggests relatively high levels of urinary expression. [score:3]
Out of the 14 miRNAs that were detected to be differentially expressed using NGS (Table  4), five (rno-let-7d-5p, rno-miR-100-5p, rno-miR-203a-3p, rno-miR-21-5p, rno-miR-320-3p) were represented on the TLDA-A, while nine (rno-miR-378a-3p, mmu-miR-5100, rno-miR-30e-3p, rno-miR-125b-2-3p, rno-miR-320-5p, rno-miR-3473, rno-miR-21-3p, rno-miR-455-5p, and hsa-miR-7641) were not. [score:3]
miRNAs identified by both platforms, let-7d, miR-203, and miR-320, may potentially serve as promising novel urinary biomarkers for drug induced renal tubular epithelial injury. [score:1]
Specifically, two out of the three miRNAs common to both qPCR and NGS approaches (let-7d and miR-320) mapped to this function (Figure  5A). [score:1]
Three miRNAs, rno-miR-320-3p, rno-miR-203a-3p, and rno-let-7d-5p, were found to be significantly altered by both the qRT-PCR and in the gentamicin treated urine specimens. [score:1]
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10
[+] score: 16
Eleven of the altered miRNAs were downregulated (miR-122, miR-93*, miR-872, miR-7*, miR-146a, miR-342-3p, miR-150, miR-139, miR-30a, miR-30e, miR-320), whereas three miRNAs, namely miR-463*, miR-34c* and miR-1188, were upregulated in the RYGB group. [score:7]
In particular, miR-342-3p, miR-320, miR-139-5p and miR-146a were predicted to be involved in multiple neurological transmitter and receptor-related pathways, as well as two major neurodegenerative disease -associated pathways (Parkinson's and Huntingtons diseases), suggesting that RYGB surgery may modulate neurological activity through a miRNA -mediated gut-brain axis. [score:5]
Decreased plasma levels of miR-342-3p, miR-320, miR-139-5p and miR-146a observed in our study suggest RYGB surgery impact on multiple neurodegenerative disease-related pathways. [score:3]
Furthermore, miR-206, miR-1188, miR-1971 and miR-34c* are inversely correlated with plasma lipid fractions, whereas miR-320 and miR-342-3p and to a lesser extent miR-7*, exhibit a positive correlation. [score:1]
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11
[+] score: 12
Song, C. L. et al. Down-regulation of microRNA-320 suppresses cardiomyocyte apoptosis and protects against myocardial ischemia and reperfusion injury by targeting IGF-1. Oncotarget, doi:10.18632/oncotarget. [score:12]
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12
[+] score: 12
The Effect of 2 Weeks of CMS on the Expression Levels of miR-18a-5p, miR-34a-5p, miR-135a-5p, miR-195-5p, miR-320-3p, miR-674-3p, and miR-872-5p in Mesocortical Pathway. [score:3]
In case of miR-320-5p and miR-872-5p in PCx, we observed that resilient animals were even more reactive to stress than anhedonic-like rats that was reflected by statistically significant change in the expression of both mentioned above miRNAs in resilient animals as compared to anhedonic-like group of rats. [score:2]
Moreover, statistical analysis showed that stress exposure for two consecutive weeks also decreased the expression levels of all examined miRNAs (except miR-34a-5p, see Fig. 3b) in rat PCx (Fig. 3a, c–f) as compared to control group of rats (miR-18a-5p F [2,29] = 14.19, p < 0.0001; miR-135a-5p F [2,29] = 16.95, p < 0.0001; miR-195-5p F [2,29] = 4.13, p < 0.02; miR-320-3p F [2,29] = 10.57, p < 0.001; miR-674-3p F [2,29] = 4.03, p < 0.05; miR-872-5p F [2,29] = 15.67, p < 0001). [score:2]
One-way ANOVA revealed increased expression levels of all miRNAs of interest (except miR-135a-5p, see Fig. 3c) after 2 weeks of CMS in VTA (Fig. 4a, b, d–g) of stressed animals as compared to non-stressed group of rats (miR-18a-5p F [2,29] = 4.34, p < 0.05; miR-34a-5p F [2,29] = 8.03, p < 0.01; miR-195-5p F [2,29] = 12.88, p < 0.001; miR-320-3p F [2,29] = 11.31, p < 0.001; miR-674-3p F [2,29] = 19.99, p < 0.0001; miR-872-5p F [2,29] = 18.18, p < 0.0001). [score:2]
Dynamic Changes in the Serum Levels of miR-18a-5p, miR-34a-5p, miR-135a-5p, miR-195-5p, miR-320-3p, miR-674-3p, and miR-872-5p during 2 Weeks of the CMS Procedure. [score:1]
Based on our previous study [20] and literature survey, we chose a set of seven different miRNAs (i. e., miR-18a-5p, miR-34a-5p, miR-135a-5p, miR-195-5p, miR-320-3p, miR-674-3p, miR-872-5p) which are associated with stress response and functioning of the central nervous system. [score:1]
Decreased plasma level of miR-320-3p has been observed in depressed and drug-naïve patients [12]. [score:1]
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13
[+] score: 11
miR-320 was downregulated after I/R in murine hearts, and knockdown of miR-320 reduced I/R -induced cardiomyocyte apoptosis by suppressing Hsp20 [13]. [score:7]
Knockdown of endogenous miR-320 protects against I/R -induced cardiomyocyte death and apoptosis by targeting heat shock protein 20 (Hsp20) [13]. [score:4]
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14
[+] score: 11
In the DRGs, 6 miRNAs (miR-9, miR-320, miR-324-3p, miR-672, miR-466b, and miR-144) were significantly downregulated in the entrapment group and 3 miRNAs (miR-9, miR-320, and miR-324-3p) were significantly downregulated in the decompression group. [score:7]
In the DRGs, 6 miRNAs in the entrapment group (miR-9, miR-320, miR-324-3p, miR-672, miR-466b, and miR-144) and 3 miRNAs in the decompression group (miR-9, miR-320, and miR-324-3p) were significantly downregulated. [score:4]
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15
[+] score: 9
We then used a screening system based on the luciferase reporter plasmid carrying the full-length 3′UTR of the FSHb mRNA and found that 18 miRNAs, specifically miR-433-3p, miR-323-3p, miR-328a-3p, miR-3573-3p, miR-204-5p, miR-206-5p, miR-31a-5p, miR-7a-5p, miR-880-3p, miR-186-5p, miR-503-5p, miR-383-5p, miR-324-5p, miR-505-5p, miR-27b-3p, miR-221-5p, miR-320-3p and miR-21-3p, could suppress the expression of the reporter by more than 30% (Figure 1). [score:5]
Interestingly, we identified 12 other miRNAs (miR-323-3p, miR-328a-3p, miR-3573-3p, miR-204-5p, miR-206-5p, miR-31a-5p, miR-7a-5p, miR-880-3p, miR-186-5p, miR-503-5p, miR-383-5p and miR-320-3p) that might also regulate FSHb expression, and then affected FSH secretion, but their specific effects need to be verified through further experiments. [score:4]
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16
[+] score: 8
Although it did not meet the criteria of two-fold or greater increased expression, miR-320-3p demonstrated significantly increased expression in the Cd-treatment group. [score:5]
Previous research has identified β-catenin mRNA as a target of miR-320 [52]. [score:3]
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17
[+] score: 7
MiR-320 was down-regulated, while miR-21, miR-146b and miR-491 were up-regulated after IR injury [16]. [score:7]
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18
[+] score: 7
In the mo del group, 17 miRNAs were downregulated, including miR-1, miR-133, miR-29, miR-126, miR-212, miR-499, miR-322, miR-378, and miR-30 family members, whereas the other 18 miRNAs were upregulated, including miR-21, miR-195, miR-155, miR-320, miR-125, miR-199, miR-214, miR-324, and miR-140 family members. [score:7]
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19
[+] score: 6
Nevertheless, changes in the levels of miR-29a-3p, miR-30c-2, and miR-320 were not significantly affected by Ucn-1. To assess the endogenous expression of miR-125a-3p, miR-324-3p, and miR-139-3p, we treated isolated cardiac myocytes with different concentrations of Ucn-1 (2, 10 and 50 nM). [score:3]
To validate microarray results, we further examined the expression of miRNAs using qRT-PCR in samples from Langendorff-perfused hearts undergoing the same protocol as in Fig.   1. We focused on 6 miRNAs, miR-30c-2, miR-29a-3p, miR-125a-3p, miR-139-3p, miR-320, and miR-324-3p, which role in cardioprotection is still unknown. [score:3]
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20
[+] score: 6
Ren et al. applied a well-established cardiac ischemia/reperfusion (I/R) mo del to determine the miRNA expression signature in ischemic hearts, and found that knockdown of endogenous miR-320 provided protection against I/R -induced cardiomyocyte death and apoptosis by targeting a well-studied cardioprotector HSP20 [10]. [score:6]
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21
[+] score: 5
Apart from regulating structure of BSCB, some studies have showed that protective effects of miR-320 involved in regulation heat shock protein-20 by inhibiting apoptosis during IR [35, 36]. [score:5]
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22
[+] score: 5
MiRNA-21 (A), miRNA-199a (B), miRNA-130b (C), miRNA-138-1 (D), miRNA-9 (E), miRNA-27a (F), miRNA-125a (G), and miRNA-320 (H) expression was not validated at 3 days after treatment with BM-MSC. [score:3]
In recent studies, miRNAs, including miRNA-15b [14], miRNA-34a [15], miRNA-92a [16], and miRNA-320 [17] have been reported to be involved in the regulation of cardiomyocyte apoptosis after MI. [score:2]
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23
[+] score: 5
Over -expression of miR-320 increases cardiomyocyte death and apoptosis by targeting heat-shock protein 20 [15]. [score:5]
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24
[+] score: 5
Some miRNAs such as miR-24, miR-186, let-7f and miR-320 showed changes in expression throughout all time points (Figure S2C). [score:3]
Among these miRNAs with shared directions of change in in vitro cultured hippocampal neurons and in vivo hippocampal CA1 regions after either neuronal stimulation or contextual conditioning were miR-24, miR-326, miR-320, miR-21 and miR-10b. [score:2]
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25
[+] score: 3
Compared to the other 2 groups, 21 miRNAs are upregulated in 6-hour group as shown in the upper portion of Fig. 2, miR-9, miR-204, miR-335, miR-23a, miR-708, miR-146a, miR-325-5p, miR-106b, miR-143, miR-140, miR-376b-3p, miR-7a, miR-541, miR-185, miR-499, miR-127*, miR-320, miR-140*, miR-145*, miR-423*, miR-378. [score:3]
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26
[+] score: 2
It has been observed that many miRNAs regulate cell apoptosis, such as miR-1, miR-133, miR-199, miR-208, miR-320, miR-21, and miR-204, etc [18- 23]. [score:2]
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27
[+] score: 2
According to our in silico analysis, Ppar γ is likely regulated by microRNAs like let-7 family members, miR-30 family members, miR-27b, miR-23ab, miR-93, miR-25, miR-128ab, miR-320, and miR-135. [score:2]
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An assessment of the degree of conservation for structure-specific distribution of microRNAs in Wistar rat, Beagle dog and cynomolgus monkey (see for relative enrichment analysis), revealed high enrichment of nine microRNAs cardiac valves (miR-let7c, mIR-125b, miR-127, mir-199a-3p, miR204, miR-320, miR-99b, miR-328 and miR-744) (Figure 3A) and seven microRNAs in the myocardium (miR-1, mir-133a, miR-133b, miR-208b, miR-30e, miR-499-5p, miR-30e*) (Figure 3A). [score:1]
Conserved microRNA signatures were identified in valves (miR-let-7c, miR-125b, miR-127, miR-199a-3p, miR-204, miR-320, miR-99b, miR-328 and miR-744) and in ventricular-specific regions of the myocardium (miR-1, miR-133b, miR-133a, miR-208b, miR-30e, miR-499-5p, miR-30e*) of Wistar rat, Beagle dog and cynomolgus monkey. [score:1]
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The selected miRNAs were rno-let-7a (part # 4373169), rno-miR-132 (part # 4373143), rno-miR-206 (part # 4373092) and rno-miR-320 (part # 4395388). [score:1]
The within-region variability of miR-132 (sd = 0.38 and 0.37), miR-320 (sd = 0.38 and 0.44), miR-497 (sd = 0.47 and 0.27) and let-7a (sd = 0.40 and 0.55) did not differ from the regional average of the hippocampus (sd = 0.39) and the hypothalamus (sd = 0.43) respectively (P-values from 0.13 to 0.95). [score:1]
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miR-21, a marker of vascular smooth muscle cell proliferation and apoptosis, was also included along with miR-126, an endothelial marker, and miR-320, which is linked to ischemia and infarction [24- 26]. [score:1]
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Furthermore, many miRNAs have been reported to play a role in diabetic heart, such as miR-1 [9], miR-133a [10], and miR-320 [11]. [score:1]
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There are some agents or methods used to protect myocardial I/R injury, such as insulin, bradykinin, atorvastatin, microRNA-320, cyclosporine, ischemia preconditioning, ischemia postconditiong and so on [3]. [score:1]
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Furthermore, three circulating plasma miRNAs (miR-16, miR-320, and miR-210) have been identified in acute kidney injury (AKI) patients as potential renal biomarkers [16]. [score:1]
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Specially, several miRNAs including miRNA-320 [15], miRNA-21 [16] and miRNA-494 [17] are involved in myocardial ischemia. [score:1]
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Wang X Cardiomyocytes mediate anti-angiogenesis in type 2 diabetic rats through the exosomal transfer of miR-320 into endothelial cellsJ. [score:1]
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Comparison of whey qPCR analyses using the same volumes of samples showed that levels of some miRNAs, such as let-7c, miR-29a, miR-29c, miR-192, miR-21, miR-146a, miR-150, miR-223, and miR-320, did not change during the lactation period (Fig. 6). [score:1]
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Other miRs which were more abundant in CDC-EVs vs MSC-EVs included miR-124, miR-210, miR-92 and miR-320. [score:1]
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