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7 publications mentioning rno-mir-352

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-352. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 281
Furthermore, our in vitro experiments demonstrate that inhibition or overexpression of miR-352 results in the up-regulation or down-regulation of IGF2R expression in endothelial cells respectively. [score:13]
The main findings of this study areas follows: (1) a different miRNA expression profile exists in collateral vessels induced by elevated FSS in the rat AV-shunt mo del; (2) miR-352 is down-regulated and has an anti-arteriogenic role in FSS -induced collateral vessel growth; (3) miR-352 regulates autophagy through regulating its target gene IGF2R/CI-M6P during arteriogenesis in a rat AV-shunt mo del. [score:10]
On the other hand, inhibition of miR-352 in vivo led to an up-regulation of IGF2R expression and increased autophagic activity in collaterals, which was indicated by increased expression of several autophagy-related genes, including Beclin1, ATG5 and LC3. [score:10]
Notably, treatment with miR-352 inhibitor + siIGF2R or inhibitor cont + siIGF2R significantly reduced both endothelial tube formation and cell proliferation in cultured RAECs as compared to treatment with miR-352 inhibitor + siNC or inhibitor + siNC, respectively, indicating that IGF2R is a miR-352 target in RAECs (*** P < 0.001, * P < 0.05, n = 3). [score:10]
Overexpression of miR-352 reduced IGF2R expression on both the mRNA and protein level in RAECs, whereas knockdown of miR-352 resulted in a significant up-regulation of IGF2R (Fig.   4C–E). [score:9]
We found that treatment with miR-352 inhibitor + siIGF2R or Inhibitor cont + siIGF2R significantly reduced both endothelial tube formation and cell proliferation in cultured RAECs compared to those in RAECs treated with miR-352 inhibitor + siNC or inhibitor + siNC (Fig.   5). [score:8]
Indeed, we found that in AV-shunt collaterals down-regulation of miR-352 expression was accompanied by increased IGF2R expression. [score:8]
Transfection of miR-352 mimic inhibited luciferase activity, whereas mutant or mimic control had no effect (Fig.   4B), indicating that miR-352 can down-regulate IGF2R expression by binding to its 3′-UTR. [score:8]
Because we found that miR-352 regulated IGF2R expression in vitro and because the literature showed that miR-352 is involved in the lysosomal-autophagy pathway, our next aim was to test whether inhibition of miR-352 altered the expression of IGF2R, IGF2, Beclin1, LC3a, LC3b and ATG5 in vivo. [score:8]
We determined that miR-352 is expressed in endothelial cells and inhibits arteriogenesis in vivo and angiogenesis in vitro via regulating its target gene insulin-like growth factor II receptor/ cation-independent mannose 6-phosphate (IGF2R/CI-M6P). [score:8]
We found that overexpression of miR-352 suppressed endothelial cell proliferation, migration and network formation, whereas inhibition of miR-352 promoted endothelial network formation, cell migration and proliferation, suggesting an anti-angiogenic potency of miR-352. [score:7]
qPCR showed that miR-352 expression was strongly increased at 24 hours after transfection with miR-352 mimic, whereas transfection with miR-352 inhibitor resulted in a significant decrease in miR-352 expression (Figure  S6). [score:7]
Given that miR-352 regulates angiogenesis and arteriogenesis, that all three bioinformatics algorithms predicted that IGF2R has a binding site for miR-352 and that IGF2R was up-regulated in collateral vessels by elevated FSS in a rabbit mo del [8], we considered IGF2R to be an important potential target. [score:6]
Therefore, we propose that miR-352 regulates autophagy during collateral vessel growth by targeting IGF2R expression. [score:6]
To verify whether IGF2R is involved in regulating the autophagic activity induced by miR-352 inhibition, the ratio of LC3II to LC3I was measured in RACEs treated with miR-352 mimic, miR-352 inhibitor, siIGF2R or miR-352 inhibitor plus siIGF2R. [score:6]
We first used the in situ-hybridization approach to localize the cells that express miR-352 in collaterals and found that both, endothelial and smooth muscle cells express miR-352. [score:5]
Differential expression of miRNAs in collateral vessels and the miR-352 expression pattern. [score:5]
The results of the qRT-PCR experiment showed that miR-352 expression was constant in each sample and confirmed our microarray data, which showed that miR-352 was expressed in collateral vessels on ligation side and significantly decreased in shunt side (Fig.   1B). [score:5]
RAECs were transfected with either miR-352 mimic, miR-352 inhibitor or the respective negative controls: mimic control/inhibitor control. [score:5]
miR-352 has anti-angiogenic potency in vitroTo investigate the potential role of miR-352 in angiogenesis, we used miR-352 mimic and inhibitor, respectively to overexpress and inhibit miR-352 in cultured rat aorta endothelial cells. [score:5]
qPCR showed that antagomir-352 treatment resulted in a strong suppression of miR-352 expression in collateral vessels (Figure  S8B). [score:5]
To investigate the potential role of miR-352 in angiogenesis, we used miR-352 mimic and inhibitor, respectively to overexpress and inhibit miR-352 in cultured rat aorta endothelial cells. [score:5]
Figure 2Effect of miR-352 overexpression or inhibition on angiogenesis in cultured rat aorta endothelial cells (RAECs). [score:5]
Using in situ hybridization and immunofluorescence for vascular markers, including a hybridization probe against U6 as a positive control, and a hybridization probe against miR-159 was used as a negative control (because this miRNA is not expressed in rat tissue), we found that miR-352 was mainly expressed in the endothelium and tunica media of collaterals and was significantly decreased in shunt-side collateral vessels (Fig.   1C). [score:5]
On the other hand, we found that the ratio of LC3II to LC3I was significantly lower in the RACEs treated with miR-352 inhibitor plus siIGF2R, as compared to those treated with miR-352 inhibitor (Figure  S11), indicating that the miR-352-IGF2R pathway may regulate autophagy during collateral vessel growth. [score:5]
In the miRNA expression profile, we found several miRNAs including miR-352, that have not been previously described as regulators in vascular biology. [score:4]
However, it should be noted that although miRNAs-including miR-352 in this paper and other miRNAs found in previous studies, such as miR-100, miR-155, miR-329, and miR-495- are important factors controlling FSS -induced collateral vessel growth 15– 17, the mechanism by which miRNAs expression is regulated remains unclear. [score:4]
In contrast, the inhibition of miR-352 resulted in an increase in endothelial cell network formation (Fig.   2A), cell migration (Fig.   2B) and cell proliferation (Fig.   2C). [score:3]
Furthermore, using the in vivo antagomir approach, we demonstrated that inhibition of miR-352 promotes cell proliferation, collateral vessel growth and collateral flow restoration after femoral ligature in the rat hind limb. [score:3]
miR-352 mimic attenuated cell migration, whereas inhibition of miR-352 promoted cell migration. [score:3]
org]), and identified 15 genes with a miR-352 target site predicted by all three bioinformatic algorithms (Figure  S4); one of them is IGF2R. [score:3]
Based on the previous results, we tested whether inhibition of miR-352 promotes collateral vessel growth in vivo. [score:3]
Figure 1Expression of miR-352 in collateral vessels of the ligature-only side (LO) and the AV-shunt side (AVS). [score:3]
IGF2R is a target of miR-352. [score:3]
Figure 3Inhibition of miR-352 enhances arteriogenesis and promotes flow restoration in rat hind limbs. [score:3]
Ligature: the ligature-only side; Shunt: the AV shunt side; antagomir-352: rats infused with antagomirs targeting miR-352 through an osmotic mini pump connected to the proximal region of the occluded femoral artery; and antagomir-cont: control antagomir. [score:3]
org]) to screen potential miRNA seed sequences in the 3′-UTR and identified IGF2R, which has a potential miR-352 target site that was predicted by all bioinformatic algorithms. [score:3]
In addition, Ki67 staining of collateral vessels revealed an increased proliferative activity of the vascular cells after miR-352 inhibition (Fig.   3B). [score:3]
Analysis using 3 bioinformatic algorithms predicted that IGF2R is the target of miR-352. [score:3]
We identified that miR-352 is a novel candidate that negatively regulates collateral vessel growth and demonstrated that miR-352 is an endogenous IGF2R modulator in the regulation of angiogenesis and autophagy. [score:3]
miR-352 mimic attenuated angiogenic tube formation, whereas inhibition of miR-352 had a stimulatory effect. [score:3]
These data lead to the conclusion that miR-352 is not only an anti-angiogenic regulator but also an anti-arteriogenic regulator. [score:3]
Luciferase activity of the IGF2R wt 3′-UTR construct but not the IGF2R mut construct, was decreased in the miR-352 -expressing cells (* P < 0.05, n = 3). [score:3]
Figure 4Identification of IGF2R as a target of miR-352 in rat aorta endothelial cells (RAECs). [score:3]
miR-352 mimic attenuated cell proliferation, whereas miR-352 inhibitor promoted cell proliferation (* P < 0.05, n = 3). [score:3]
To examine the biological relevance of reduced IGF2R by miR-352, we tested endothelial tube formation and cell proliferation in cultured RAECs treated with miR-353 inhibitor versus siIGF2R. [score:3]
On the other hand, of those differentially expressed miRNAs, a few have not previously been described or have been rarely reported, for example, miR-352. [score:3]
We found that inhibition of miR-352 increased the LC3II/LC3I ratio, whereas miR-352 mimic reduced the LC3II/LC3I ratio (Figure  S11). [score:3]
Moreover, an increase in IGF2R expression in collaterals was evident after miR-352 gene silencing. [score:3]
Inhibition of miR-352 by antagomir treatment promotes collateral vessels growth and collateral flow restoration in rat hind limbs. [score:3]
Most recently, Tao et al. showed that miR-352 regulates autophagy following ischaemic stroke [20]. [score:2]
To test whether miR-352 directly regulates IGF2R, we used a dual-luciferase reporter assay in RAECs transfected with either wild-type or mutated IGF2R 3′-UTR firefly luciferase constructs and miR-352 mimic or negative mimic control. [score:2]
Therefore, we speculated that miR-352 could regulate angiogenesis and arteriogenesis. [score:2]
It should be noted that the miR-352-IGF2R pathway may not be the only mechanism for regulating autophagy during collateral vessel growth because additional miRNAs involved in autophagy were identified, such as, miR-30. [score:2]
Next, we identified miR-352 as the most consistently down-regulated miRNA and investigated its localization in collateral vessels as well as its functions in collateral vessel growth. [score:2]
The overexpression of miR-352 resulted in a decrease in endothelial cell network formation in the planar Matrigel (Fig.   2A), cell migration (Fig.   2B) and cell proliferation assays (Fig.   2C). [score:2]
All the above-mentioned findings indicate that miR-352 could be a novel miRNA regulator of elecated FSS -induced-collateral vessel growth. [score:2]
These findings confirm that IGF2R is negatively regulated by miR-352. [score:2]
These indicated that IGF2R is regulated by miR-352 in RAECs. [score:2]
To determine whether miR-352 is a novel candidate that regulates collateral vessel growth, we used 3 bioinformatic algorithms (miRanda [www. [score:2]
Notably, miR-352 was present mainly in endothelial and smooth muscle cells of the collateral vessels, and its expression was decreased in collateral vessels of the AVS as compared with those in the LO. [score:2]
miR-352 was modulated in vivo after femoral ligature by the additional application of antagomir-352 via osmotic mini pumps for a period of one week (Figure  S8A). [score:1]
Furthermore, using qPCR, western blotting and immunofluorescence, we investigated the direct regulation of IGF2R by miR-352 in RAECs. [score:1]
To our knowledge, the only available information about the function of miR-352 was reported in Tao’s study, which showed that miR-352 is involved in the lysosomal-autophagy pathway [20]. [score:1]
miR-352 was first found in E18 rat primary cortical neurons [31]. [score:1]
Taken together, these data demonstrate that the miR-352-IGF2R pathway is involved in angiogenesis and arteriogenesis. [score:1]
Taken together, we concluded that miR-352 has anti-angiogenic potency in endothelial cells. [score:1]
miR-352 has anti-angiogenic potency in vitro. [score:1]
IGF2R contains a miR-352 binding site in the 3′-UTR of its mRNA (Fig.   4A). [score:1]
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[+] score: 31
We observed: i) down-regulation of miR-128a-3p in the three stages of epileptogenesis; ii) up-regulation of miR-196b-5p only at 24h post-SE, and; iii) up-regulation of miR-352 in both 24h and chronic post-SE time points. [score:10]
To verify the accuracy of microarray results we chose a selection of miRNAs from up-regulated (miR-10a-5p, miR-196b-5p, miR-352 and miR-324-3p) and down-regulated (miR-128a-3p) categories for confirmation using the method. [score:7]
An additional complication is the absence of an experimentally validated target for miR-352. [score:3]
Expression patterns of miR-128a-3p, miR-196b-5p and miR-352 during S-PILO-SE induced epileptogenesis. [score:3]
Expression Patterns of miR-128a-3p, miR-196b-5p and miR-352 in three Stages of S-PILO-SE induced epileptogenic process. [score:3]
Finally, miR-352 transcripts were significantly up-regulated in the 24h group compared with naïve, and in the chronic phase group compared with naive or 0h groups. [score:2]
This suggests that an investigation of HEXB and the identification of other direct targets would be a productive next step towards uncovering the role of miR-352 in epileptogenesis. [score:2]
Identifying a potential link between miR-352 and epilepsy is challenging because the biological role of this miR is unknown. [score:1]
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[+] score: 11
The most upregulated miRNAs were miR-146a-5p, miR-132-5p, miR-21-5p at 1.63, 1.61, and 1.56-fold of the control, respectively, while the most downregulated miRNAs were miR-29b-3p, miR-352, miR-30e-5p at 0.60, 0.70, and 0.72-fold of the control, respectively. [score:7]
We found common expression of 9 miRNAs (miR-132, miR-137, miR-139, miR-29a, miR-324, miR-352, miR-282, miR-146a, and miR-23a) when our data were compared to a data set describing miRNA expression 60 d after pilocarpine -induced status epilepticus [24]. [score:4]
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4
[+] score: 9
The top 10 miRNAs upregulated and downregulated upon treatment with Tg and Tm, respectively are shown in Figure 2B-C. The expression of miR-98, let-7d*, miR-374, miR-181d, miR-352, miR-7a and miR-26b were increased both by Tg and Tm in H9c2 cells. [score:9]
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[+] score: 7
We suppose that SFI attenuates myocardial hypertrophy by upregulating the levels of particular miRNAs, including miR-19a-3p, miR-181d-5p, miR-210-3p, miR-352 and miR-324-3p, and downregulating miR-199a-5p. [score:7]
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[+] score: 7
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-15a, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, 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-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Such a situation occurred for miR-26b, miR-30, and miR-374 downregulation, and for miR-34, miR-301, and miR-352 upregulation [121]. [score:7]
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7
[+] score: 4
Ventral combined with dorsal root avulsion resulted in a sustained upregulation of 10 miRNAs, including miR-19b-3p, miR-20b-5p, miR-21-5p, miR-27a-3p, miR-29b-3p, miR-106b-3p, miR-142-3p, miR-322-5p, miR-352, and let-7a-5p (Figure  2E). [score:4]
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