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15 publications mentioning rno-mir-322-2

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-322-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 207
Our results show that in rat PASMCs all the BMP signaling factors are downregulated in response to hypoxia and miR-322 can affect the proliferation and migration of PASMCs by directly targeting BMPR1a and Smad5. [score:7]
Hypoxia-sensing via HIF-1 upregulates the transcription of miR-322, which then exerts positive feedback by facilitating stabilization of HIF-1α by targeting the molecules involved in its degradation for ubiquitination and degradation 23. [score:6]
Hypoxia upregulates expression of miR-322 in rat PASMC and A7r5 cells. [score:6]
In addition, the reduction or increase of other BMP -associated proteins caused by either overexpression or inhibition of miR-322 is perhaps achieved through an indirect pathway. [score:6]
Hypoxia upregulates expression of miR-322 in lungs and PASMCs. [score:6]
To further assess whether HIF-1α affects the transcription of miR-322, we transfected A7r5 cells with an adenoviral vector expressing modified oxygen dependent degradation domains (ODDD-wt) that express a HIF-1α ODDD domain from amino acids 531 to 575. [score:5]
For miRNA overexpression experiments in rat PASMCs, lentiviral vectors based on pLVX-Puro backbone (Clontech, Mountain View, CA) were used to express miR-322 as described before 22. [score:5]
As shown in Fig. 2c, the expression of miR-322 was upregulated 1.6-fold in hypoxia compared to normoxia. [score:5]
Upper panel: conserved miR-322 binding sites in the 3′-UTR of Smad5 and BMPR1a along with the mutation site; Bottom panel: 3′-UTR luciferase reporter assay with targets and their mutant along with miR-322/miR-Con overexpressing vectors. [score:5]
More importantly, we found that HIF-1α upregulates the transcription of miR-322 by directly binding to the HRE site on its promoter. [score:5]
Among these, miR-322 was found to be significantly upregulated during the course of development of PH 18. [score:5]
As shown in Fig. 4b, cells with miR-322 inhibition (anti-322) exhibited significantly reduced expression in miR-322 compared to its control cells (anti-Con). [score:4]
To confirm that the regulation of miR-322 on cell proliferation and migration is achieved by targeting BMPR1a and Smad5, we carried out the following rescue experiments. [score:4]
This indicates that the HRE site within the miR-322 promoter is required for HIF-1α -induced upregulation in hypoxia. [score:4]
In this study, we have elucidated a possible mechanism by which miR-322 is upregulated in PASMCs during hypoxia. [score:4]
As shown in Fig. 7d, the proliferation and migration of rat PASMCs, which were blocked by miR-322 inhibition (anti-322 and si-Con), were significantly increased by either BMPR1a or Smad5 knockdown (si-BMPR1a or si-Smad5 together with anti-Con). [score:4]
Luciferase reporter assays with transfected 3′-UTR sequences along with miR-322 or miR-Con overexpressing vectors showed that only BMPR1a and Smad5 were repressed by miR-322 overexpression (Fig. 7b). [score:4]
Knockdown of miR-322 was achieved by using dTuD constructs against mature rno-miR-322, which was modified from TuD vector 39 with one more TuD expression cassette. [score:4]
Additional 3′-UTR mutation assays validated that miR-322 can directly target the predicted binding sites on the 3′-UTR of BMPR1a and Smad5 (Fig. 7c). [score:4]
Left: representative western blot for hypoxia -dependent decrease of BMP signaling factors; Middle and right: Overexpression/ knockdown of miR-322 altered the protein level of factors in BMP signaling. [score:4]
The results showed that the expression of miR-322 and miR-351 was increased significantly with the duration of hypoxia exposure (Fig. 1b). [score:3]
Next we determined whether hypoxia -induced expression of miR-322 in rat lung and in vitro cultured PASMCs parallels the mouse lung miRNA profile. [score:3]
Here, we confirmed the hypoxia -induced increase in expression of miR-322 in rat PASMCs, highlighting miR-322 as the functional hypoxamirs in PASMCs. [score:3]
Since HIF-1 and -2 mediate most of the cellular responses to hypoxia, we hypothesized that the hypoxia -induced increase in expression of miR-322 is HIF-related. [score:3]
Therefore, we determined whether manipulating miR-322 expression could affect the levels of HIF-1α in rat PASMCs. [score:3]
were transfected with recombinant lentiviral particles expressing miR-322 (miR-322) or control lentiviral vector (miR-Con), or with lentivirus of dTud construct against mature miR-322 (anti-322) or scramble control vector (anti-Con). [score:3]
While, together transfection with si-BMPR1a or si-Smad5 almost completely rescued the proliferative and migratory repression caused by miR-322 inhibition. [score:3]
We further tested the roles of HIF-1α and -2α in regulation of miR-322 promoter activity using a gene knockdown approach. [score:3]
Western blot showed that the accumulation of HIF-1α increased in the nucleus when overexpressing miR-322 in normoxia (Fig. 4c). [score:3]
As shown in Fig. 3c, shRNA targeting of HIF-1α almost completely abolished the activation of miR-322 promoter reporter induced by CoCl [2], but HIF-2α silencing had no effect. [score:3]
How to cite this article: Zeng, Y. et al. Hypoxia inducible factor-1 mediates expression of miR-322: potential role in proliferation and migration of pulmonary arterial smooth muscle cells. [score:3]
Notably, the protein levels of BMPR1a, BMPR2, Smad5 and ID2 were decreased in miR-322 overexpressing cells under normoxia (Fig. 7a, middle panel). [score:3]
As shown in Fig. 3e,f, qRT–PCR and western blotting revealed that the endogenous expression levels of miR-322 also dramatically increased with HIF-1α accumulation. [score:3]
In these cells miR-322 expression was increased about 2.2-fold in hypoxia. [score:3]
The influence on the miR-322 promoter reporter activity (d) and the endogenous expression levels (e) of miR-322 were determined by real-time PCR. [score:3]
were transfected with recombinant lentivirus expressing miR-322 (miR-322), or no miRNA sequence as a negative control (miR-Con). [score:3]
These results suggest that hypoxia -induced miR-322 may play a regulatory role in PASMC proliferation and migration via the BMP signaling pathway. [score:2]
This indicates a positive feedback loop regulation between HIF-1α and miR-322 in pulmonary arterial smooth muscle cell, as shown in Fig. 8. However, HIF-2α seems not to be participating in this network. [score:2]
miR-322 is transcriptionally regulated by HIF-1α. [score:2]
qRT-PCR revealed an over 12-fold increase in miR-322 in the cells overexpressing miR-322 compared with control cells (Fig. 4b). [score:2]
Altogether, the results above demonstrated that miR-322 is transcriptionally regulated by the hypoxia-responsive factor HIF-1α in hypoxia. [score:2]
miR-322 regulates BMP mediated signaling. [score:2]
To understand if the effect of miR-322 on BMP signaling is direct, we searched for potential binding sites on the 3′-UTR of the above proteins. [score:2]
Taken together these results indicate that hypoxia -induced miR-322 is involved in regulating the stability of HIF-1α in PASMCs. [score:2]
Dysregulation of BMP signaling by increased miR-322 promotes the proliferation and migration of PASMCs. [score:2]
Validation of miR-322 targets was carried out using a 3′ UTR activity assay with a similar firefly/renilla luciferase reporter system (Promega, Madison, WI). [score:2]
were also transfected with dTud constructs for miR-322 knockdown studies. [score:2]
And they were all increased by miR-322 knockdown (Fig. 7a, right panel). [score:2]
To understand the consequences of increased miR-322 in hypoxia, we investigated the effects of miR-322 overexpression and knockdown on the proliferation and migration in rat PASMCs. [score:2]
were transduced with shRNA targeting HIF-1α (shHIF-1α) or HIF-2α (shHIF-2α) and miR-322 promoter activity was determined in the luciferase reporter assay after transfection of wild type and mutant constructs and CoCl [2] treatment (left panel) as described under Methods; Control (sh-Con) or HIF-1α/-2α shRNA -transfected cells were harvested for protein analysis by western blot to determine knockdown specificity (right panel); *p < 0.05 compared with sh-Con. [score:2]
Taken together these results confirm that the positive role of miR-322 on PASMCs proliferation and migration could be fulfiled by post-transcriptionally regulating BMPR1a and Smad5. [score:2]
Using chromatin immunoprecipitation (ChIP) assay, we determined the binding of HIF-1α to the miR-322 promoter with and without CoCl [2] treatment or with ODDD-wt/-mut overexpression. [score:2]
Mo del depicting the regulation of miR-322 in PASMCs response to hypoxia. [score:2]
Knockdown of miR-322 abolished the stabilization of HIF-1α in PASMCs under hypoxic condition (Fig. 4c). [score:2]
The ChIP assays indicated that HIF-1α directly binds to the HRE site on the miR-322 promoter in vitro. [score:1]
As shown in Fig. 2a, miR-322 level in rat lungs was increased about 2-fold after 3-weeks hypoxic treatment. [score:1]
We constructed both wild and HRE-mutant promoter -driven luciferase reporter plasmids (pGL4-P1k and pGL4-P1km, respectively) and transfected A7r5 cells to determine whether HIF-1/2α influences the miR-322 promoter activity. [score:1]
miR-322 facilitates stabilization of HIF-1α. [score:1]
miR-322 promotes migration of PASMCs. [score:1]
Hypoxia induces miR-322 promoter activity in a HIF-1α -dependent manner. [score:1]
Ghosh et al. have demonstrated that the human homolog of miR-322, has-miR-424, specifically increased in endothelial and vascular smooth muscle cells, but not in tumor cell lines, in response to hypoxia 23. [score:1]
We also measured protein levels of these molecules involved in BMP signaling after overexpressing or silencing miR-322. [score:1]
Taken together these data demonstrate that hypoxia -induced miR-322 can promote migration of PASMCs. [score:1]
We searched for hypoxia-responsive elements (HRE) in the putative promoter sequence, 1000 bp upstream from the rat pre-miR-322. [score:1]
As shown in Fig. 5a, stable overexpression of miR-322 significantly accelerated the proliferation rate of PASMCs compared to its control cells both under normoxia and hypoxia by MTS assay. [score:1]
As shown in Fig. 6, the decrease in the width of the scratched wound was larger (~ 60%) in miR-322 transfected cells than in control cells after 24 h (Fig. 6a,b), and knockdown of miR-322 led to a slower decrease in wound healing compared with anti-Con transfection (~ 40%) after 24 h (Fig. 6c,d). [score:1]
All these data emphasize that miR-322 may affect the BMP signaling pathway to exert their pro-proliferation and pro-migratory activities in PASMCs. [score:1]
Luciferase activities were measured at 48 h after cotransfecting with the 3′-UTR constructs and the miR-322 overexpressing vectors or its vector control. [score:1]
In this study, we found that miR-322 can also stimulate the accumulation of HIF-1α in PASMCs. [score:1]
org), putative seed match of miR-322 was predicted within the 3′- UTR of BMPR-2, BMPR1a, Smad5, and Smad4. [score:1]
miR-322 stimulates the accumulation of HIF-1α. [score:1]
miR-322 is induced by hypoxia in mouse lung. [score:1]
These data indicate that miR-322 can significantly accelerate the proliferation of PASMCs. [score:1]
The results show that the native promoter but not the mutant promoter of miR-322 was activated by CoCl [2] (Fig. 3b). [score:1]
The relative levels of miR-322 was estimated by real-time PCR. [score:1]
Our data show that miR-322 promotes the proliferation and migration of rat PASMCs both under normoxia and hypoxia. [score:1]
miR-322 promotes proliferation of PASMCs. [score:1]
Ghosh et al. have reported that human miR-424, the homolog of rodent miR-322, stabilizes HIF-1α leading to its accumulation in the nucleus in human umbilical vein endothelial cells (HUVEC) 23. [score:1]
miR-322 promotes hypoxia -induced proliferation and migration in PASMCs. [score:1]
miR-322 participates in hypoxia -mediated BMP signaling. [score:1]
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2
[+] score: 9
According to this observation, Caruso et al. (2010) showed that, during the onset of pulmonary arterial hypertension (PAH) after hypoxia, there is a reduced Dicer expression leading to miR-22, miR-30, and let-7f down-regulation and, at the same time, to miR-322 and miR-451 up-regulation in two different PAH rat mo dels. [score:9]
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[+] score: 9
miR-322 that upregulated in leptin -deficient obese (ob/ob) mice has a cardioprotective effect by modulating the insulin pathway [21]. [score:4]
We found that miR-322-5p was one of these up-regulated miRNAs (greater than 2-fold changes) (Fig.   4a,b). [score:4]
The arrow indicates miR-322-5p. [score:1]
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4
[+] score: 9
In response to 4 hours of mechanical stretch, rno-miR-322, let-7f, miR-103, miR-126, miR-494, miR-126*, miR-130b and miR-195 were significantly dysregulated (Fig.   7A and Supplementary Dataset  5), so we sought potential mRNA targets for these dysregulated miRNAs among the stretch-regulated genes in 4 and 12 hours timepoints. [score:6]
In response to 1 hour of mechanical stretching, only one miRNA, rno-miR-130b showed differential expression compared to controls (P < 0.05), whereas 8 miRNAs (rno-miR-322, rno-let-7f, rno-miR-103, rno-miR-126, rno-miR-494, rno-miR-126*, rno-miR-130b, rno-miR-195; P < 0.05) were dysregulated in response to 4 hours of stretch (Supplemental Dataset  5). [score:3]
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5
[+] score: 8
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, 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-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, 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-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
Both ACTH and 17α-E2 up-regulated the expression of miRNA-212, miRNA-132, miRNA-154, miRNA-494, miRNA-872, miRNA-194, and miRNA-24-1, but reduced the expression of miRNA-322, miRNA-20b, miRNA-339, miRNA-27a, miRNA-551b, and miRNA-1224. [score:8]
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[+] score: 8
Of these miRNAs, rno-miR-129-1-3p, rno-miR-153-3p, rno-miR-29b-3p, rno-miR-29c-3p and rno-miR-451-5p were down-regulated, whereas rno-let-7a-1-3p, rno-miR-322-5p, rno-miR-3574 and rno-miR-628 were observed to be highly upregulated with p < 0.01 (Fig.   3). [score:7]
9 miRNAs (rno-miR-129-1-3p, rno-miR-153-3p, rno-miR-29b-3p, rno-miR-29c-3p, rno-miR-451-5p, rno-let-7a-1-3p, rno-miR-322-5p, rno-miR-3574 and rno-miR-628) showed statistically significant change. [score:1]
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[+] 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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8
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, 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-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Similarly, within the differentially expressed pool of miRNAs, 10 were identified that are intimately involved in regulating intracellular trafficking pathways, including: miR-7b-5p, miR-9-5p, miR-31-5p, miR-92a-3p, miR-106-5p, miR-126-3p, miR-150-5p, miR-204-5p, miR-222-3p, and miR-322-5p (S2 Fig). [score:4]
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9
[+] 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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[+] score: 3
Expression levels of miR-17-5p, miR-21-5p, miR-126-3p, miR-145-5p, miR-150-5p, miR-204-5p, miR-223-3p, miR-328-3p, miR-424-5p (mmu-miR-322, the mouse/rat ortholog for hsa-miR-424), and miR-503-5p were evaluated. [score:1]
MiR-424 (miR-322 ortholog) was decreased ~2 fold in the lungs and PA (Fig 1A and 1B) and decreased only slightly in RV, while miR-503 slightly increased in RV with no change in plasma (Fig 1C and 1D). [score:1]
Notably, levels of miRs 17, 21, and 223 were all significantly reduced and levels of miR-424 (mmu-miR-322, the mouse/rat ortholog for hsa-miR-424) and miR-503 were significantly increased (Fig 5). [score:1]
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[+] score: 2
Among the miRNAs that undergo the greatest dynamic regulation at early time points were miR-219 and miR-140 (Figure S1A) and at the later time point were miR-322 and miR-128a (Figure S2B, 3 and 24 h). [score:2]
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[+] score: 2
Of those, 9 miRNAs (let-7c-1, miR-221-3p, miR-221-5p, miR-222-3p, mir-322-2, mir-34c, miR-384-5p, mir-496, and mir-542-1) reported consistent directional changes as our data (15, 31– 33). [score:2]
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[+] score: 1
The top-ranking miRNA in adipose tissue was miR-322 (FC = 1.91, P = 0.029 P [adjusted ]= 0.99) but it did not rank highly in the liver. [score:1]
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[+] score: 1
#   HA LA HA LA HA LA HA-LA HA-LA   subtraction method, all pools rno-miR-30d-5p 9,187 11,047 8,140 11,168 −0.121 (−1.129) 0.011 (1.011) −0.132 (0.297) <0.0017rno-miR-378b51.647.158.633.70.125 (1.136)−0.331 (−1.398)0.457 (0.533)<0.0015rno-miR-322-3p30.729.420.832.8−0.384 (−1.476)0.109 (1.116)−0.494 (0.592)<0.001X added by log2 ratio method or randomization *, all poolsrno-miR-493-3p79.866.387. [score:1]
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[+] score: 1
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-382, 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-542-2, rno-mir-542-3
These include rno-miR-195, rno-miR-125a-5p, rno-let-7a, rno-miR-16, rno-miR-30b-5p, rno-let-7c, rno-let-7b, rno-miR-125b-5p, rno-miR-221, rno-miR-222, rno-miR-26a, rno-miR-322, rno-miR-23a, rno-miR-191, rno-miR-30 family, rno-miR-21, rno-miR-126, rno-miR-23b, rno-miR-145 and rno-miR-494. [score:1]
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