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12 publications mentioning rno-mir-301a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-301a. 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: 263
Importantly, RhoA, SRF and its target genes were strongly upregulated in Cs1-ko mice where Cfl2 is upregulated and miR-301a is downregulated, suggesting a possible involvement of Cfl2 in SRF activation in vivo. [score:12]
Finally, we found a strong in vivo correlation between downregulation of miR-301a to the upregulation of Cfl2 in Cs1-ko mice (Fig 3F–3H), suggesting a possible physiological importance of miR-301a in regulating Cfl2 in the heart. [score:8]
Microarray data revealed that several microRNAs were dysregulated in Cs1-ko mice (S1 Table), including miR301a, which was maximally downregulated, whereas, miR-298 was highly upregulated in Cs1-ko mouse hearts (schematically depicted in Fig 2A). [score:8]
Similarly, inhibition of miR-301a expression effectively accelerated SRF-signaling at basal level (Fig 5G), whereas, its overexpression significantly abrogated the RhoA -mediated activation of SRF activity (Fig 5H). [score:7]
Through this screen, we identified miR-301a as the most downregulated microRNA that we found targets Cfl2, a major regulator of actin dynamics, in vitro and in vivo. [score:7]
MiR-301a was identified the most downregulated microRNA, whereas, miR-298 was highly upregulated (N = 4 each), which was confirmed in independent cohort by quantitative real-time PCR for miR-301a (B), and miR-298 (C) (N = 5 (WT), and 6 (Cs1-ko)). [score:7]
Due to the significant effect of Cfl2 and miR-301a on RhoA/SRF-signaling in C2C12 cells/NRVCM, and observed upregulation of Cfl2 and downregulation of miR-301a in Cs1-ko mice, we determined the SRF and RhoA levels in Cs1-ko mice. [score:7]
Most interestingly, we discovered Cofilin-2 as one of the putative targets of miR-301a through microRNA target database search, which we further validated through series of experiments including luciferase assays, site directed mutagenesis of possible binding sites, and by manipulation of miR-301a expressions in neonatal rat cardiomyocytes. [score:7]
Mutation in two of the four putative binding sites (binding sites at position 370 and 1030 of the 3’UTR) prevented the reduction in luciferase activity by miR-301a overexpression suggesting that these two binding sites are responsible for miR-301a effect on Cfl2 expression (Fig 3B). [score:6]
Upregulated microRNA-301a in osteosarcoma promotes tumor progression by targeting CDC14A. [score:6]
As anticipated, overexpression of miR-301a reduced while its knockdown increased Cfl2 expression determined by immunoblotting (Fig 3C–3E). [score:6]
We further validated the expression of miR-301a and miR-298 by quantitative real-time PCR (qPCR) in independent set of mouse cohort to confirm its downregulation (Fig 2B and 2C). [score:6]
Briefly, cardiomyocytes cultured on coverslips in 12x well culture plates, either transduced with Cfl2 overexpression/knockdown adenoviral particles, or transfected with miR-301a mimic/inhibitor, were washed 2x with PBS and fixed with 4% paraformaldehyde for 10 min. [score:6]
Cfl2 or miR-301a were either overexpressed or knocked-down using respective vectors, mimic, or inhibitor transfection in C2C12 cells together with a luciferase construct carrying SRF-RE driven firefly luciferase. [score:6]
0183901.g005 Fig 5Cfl2 or miR-301a were either overexpressed or knocked-down using respective vectors, mimic, or inhibitor transfection in C2C12 cells together with a luciferase construct carrying SRF-RE driven firefly luciferase. [score:6]
In contrast, downregulation of miR-301a resulted in the activation, whereas, its overexpression significantly blunted the basal as well as RhoA -mediated activation of SRF-RE signaling (Fig 5C and 5D). [score:6]
To discriminate the expression of miR-301a and Cfl2 in cardiac major cell types, we studied their expression levels in isolated fibroblasts and cardiomyocytes from neonatal rat ventricles. [score:5]
Consistently, altered expression of miR-301a by treating NRVCM with miR-301a inhibitor (G) or mimic (H) oppositely affected the luciferase activation. [score:5]
Although miR-301a is significantly expressed in the heart and other tissues, no cardiac role of this ubiquitously expressed microRNA is known yet. [score:5]
On the other hand, miR-301a targets Cfl2 in cardiomyocytes, thereby inhibiting the activation of SRF signaling. [score:5]
S2 Fig(A) Expression of miR-301a was determined in various tissues by quantitative real-time PCR indicates ubiquitous distribution of miR-301a, including significant expression in the heart (N = 3). [score:5]
Next, we used online prediction databases to identify possible miR-301a targets which resulted into hundreds of putative targets. [score:5]
Overexpression of Cfl2 or knockdown of miR-301a though resulted in the activation of SRF signaling, neither of these treatments caused hypertrophy. [score:4]
We therefore propose to explore the possibility of use of miR-301a manipulations for therapeutic intervention to target cardiac disorders caused due to deregulation of Cfl2. [score:4]
MicroRNA miR-301a is downregulated in Cs1-ko mice. [score:4]
We also found that Cfl2 increases the RhoA -mediated SRF activation, whereas, miR-301a upregulation is sufficient to antagonize these effects (Fig 7). [score:4]
To our surprise, neither overexpression nor knockdown of Cfl2 or miR-301a affected the cell size in neonatal rat cardiomyocytes (Fig 5I–5L). [score:4]
Ablation of miR-301a resulted into similar effects as observed with the Cfl2 overexpression, pertaining to the increased levels of Cfl2 upon miR-301a knockdown. [score:4]
Through a microRNA microarray we identified miR-301a is significantly downregulated in Calsarcin-1 deficient mice that present DCM phenotype in a pure C57BL/6 background. [score:4]
Knockdown of miR-301a also increased the luciferase activation (C), and the overexpression of miR-301a mimic significantly blunted the luciferase activity (D). [score:4]
These vectors were co -transfected with either Cofilin-2 or miR-301a knockdown (Negative Control siRNA, Qiagen®; Cofilin 2 siRNA (m): sc‑37026, Santa Cruz Biotechnology), or overexpression constructs (n = 6) using Lipofectamine® 2000 Transfection Reagent (Thermo Fisher Scientific) 24h after seeding the C2C12 cells. [score:4]
We therefore hypothesized that Cfl2 plays an essential role in RhoA-SRF activation and miR-301a will negatively affect this activation by regulating Cfl2 expression. [score:4]
MicroRNAs like miR-19a, 34b, 129, 135a, 142-3p, miR-153, miR-186, miR-187, and miR-301a were significantly downregulated in Cs1-ko mice. [score:4]
Similarly, siRNA mediated knockdown of Cfl2 (K) or overexpression of miR-301a too did not alter cell surface area (L). [score:4]
Tissue distribution pattern for miR-301a determined by qPCR revealed its ubiquitous expression in the heart, brain, skeletal muscle, etc. [score:3]
miR-301a targets Cofilin-2 in cardiomyocytes and in Cs1-ko mice. [score:3]
To test this hypothesis, we performed SRF-response element (SRF-RE) driven firefly luciferase activity assay by either overexpressing or knocking down Cfl2/miR-301a in C2C12 cells. [score:3]
To strengthen these in vitro findings, we found a strong inverse correlation between Cfl2 and miR-301a expression in Cs1-ko mice. [score:3]
0183901.g004 Fig 4Protein and RNA was extracted from isolated neonatal rat cardiomyocytes and fibroblasts for comparative analysis of miR-301a and Cfl2 expression status. [score:3]
We then confirmed if miR-301a targets Cfl2 in vitro in neonatal rat ventricular cardiomyocytes (NRVCM). [score:3]
Cofilin-2 is a target of miR-301a. [score:3]
Protein and RNA was extracted from isolated neonatal rat cardiomyocytes and fibroblasts for comparative analysis of miR-301a and Cfl2 expression status. [score:3]
Expression of miR-301a was modulated in NRVCM same as in C2C12 cells. [score:3]
NRVCM were transfected 24h post seeding using Lipofectamine® RNAiMAX (Thermo Fisher Scientific) to transfect microRNA miR-301a mimic/inhibitor, or a control microRNA, as per manufacturer's recommendation. [score:3]
Furthermore, our in vitro data indicated that miR-301a attenuates RhoA -mediated activation of SRF signaling via targeting Cfl2 in vitro without affecting cellular hypertrophy. [score:3]
Expression of miR-301a and Cfl2 is higher in cardiomyocytes than fibroblasts. [score:3]
MiR-301a, the most -downregulated microRNA in our screen has previously been associated strongly with many human cancers including prostate cancer, malignant melanoma, osteosarcoma, etc. [score:3]
Similar findings were observed when we modulated the expression of Cfl2 or miR-301a. [score:3]
Moreover, our in vitro data indicated that miR-301a attenuates RhoA -mediated activation of SRF signaling via targeting Cfl2 without affecting cellular hypertrophy. [score:3]
Therefore, we believe that our findings provide an important layer in Cfl2 regulation, which needs further in vivo validations for exploiting the therapeutic potential of miR-301/Cfl2 interactions in cardiac signal transduction and DCM. [score:2]
miR-301a and Cfl2 oppositely regulates Rho -mediated SRF signaling but not cellular hypertrophy. [score:2]
Knockdown of miR-301a also led to no effect on cell size (J). [score:2]
Here, we show that miR-301a regulates the expression as well as physiological function of Cfl2 in cultured cardiomyocytes, which needs additional in vivo evaluations and validation by gain- and loss-of-function studies. [score:2]
Moreover, we here found that miR-301a was highly expressed in isolated cardiomyocyte compared to fibroblasts, suggesting a cell-type specific function for this microRNA. [score:2]
Mutations in binding sites 370 and 1030 resulted in loss of luciferase activation, clearly suggesting that these two sites act as binding sites for miR-301a (N = 4). [score:2]
Expression of miR-301a and Cfl2 is higher in cardiomyocytes compared to fibroblasts. [score:2]
Functional characterization of this microRNA in cardiac perspective revealed that miR-301a targets and regulates Cfl2 in vitro in neonatal rat cardiomyocytes, and in vivo in Cs1-ko mice. [score:2]
We found four putative miR-301a binding sites in 3’UTR of Cfl2 depicted in S1A Fig which we mutated by site directed mutagenesis and studied for the validation of miR-301a binding. [score:2]
We found that the expression of both miR-301a and Cfl2 was higher (>2 fold) in cardiomyocytes compared to fibroblasts (Fig 4A–4C). [score:2]
miR-301a and Cfl2 oppositely regulates Rho -mediated SRF signaling. [score:2]
S1 FigCofilin 3’UTR contains four possible miR-301a binding sites named as 370, 890, 1030, and 1717 as presented pictorially in A. Original uncropped blots are shown for Fig 3C (B, C), and 3F (D). [score:1]
Cofilin 3’UTR contains four possible miR-301a binding sites named as 370, 890, 1030, and 1717 as presented pictorially in A. Original uncropped blots are shown for Fig 3C (B, C), and 3F (D). [score:1]
Mo del figure of cardiac role of Cfl2 and miR-301a. [score:1]
These similar in vitro findings points towards possible involvement of Cfl2-miR301a in the pathophysiology of Cs1-ko mice, at least partially. [score:1]
Tissue distribution of miR-301a. [score:1]
Putative miR-301a binding sites in 3’UTR of Cfl2. [score:1]
Transfection of miR-301/anti-miR301. [score:1]
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[+] score: 260
Other miRNAs from this paper: rno-mir-130a, rno-mir-130b, rno-mir-146a, rno-mir-301b
The up-regulation of miR-301a in breast cancer and Ewing’s sarcoma cells promotes tumor metastasis and tumor cell proliferation by targeting the tumor suppressor PTEN [44, 54]. [score:8]
We provide evidence that glycine -induced neuroprotection is mediated through the up-regulation of miR-301a and subsequent suppression of PTEN expression. [score:8]
a, qRT-PCR shows that the levels of PTEN mRNAs are down-regulated and up-regulated in the cortical neurons treated with miR-301a agomir and antagomir, respectively (n = 6, * P < 0.05 vs. [score:7]
We demonstrated that the level of PTEN mRNA was down-regulated in the cultured cortical neurons treated with miR-301a agomir for 24 h and up-regulated in the cultured cortical neurons treated with miR-301a antagomir for 24 h (Fig. 7a). [score:7]
In the present study, we provide new evidence that PTEN is negatively regulated by miR-301a and that PTEN suppression by miR-301a up-regulation mediates glycine -induced neuroprotective effect. [score:7]
It has been reported that miR-301a is up-regulated in hepatocellular carcinoma and modulates NF-kB expression by negatively regulating Gax [53]. [score:7]
The present study provides new evidence that the neuroprotective effect of glycine is mediated by the enhancement of miR-301a expression and subsequent suppression of PTEN expression in cortical neurons. [score:7]
We provided the first evidence that glycine increased the expression of microRNA-301a in cultured rat cortical neurons and protected against cortical neuronal death through up-regulation of microRNA-301a after oxygen-glucose deprivation. [score:6]
miR-301a is up-regulated in pancreatic cancer and to activate NF-kB by negative regulation of NF-kB-repressing factor gene [46]. [score:5]
MicroRNA-301a directly bound the predicted 3′UTR target sites of PTEN and reduced PTEN expression in cortical neurons. [score:5]
In addition to its effect on cancer, miR-301a is shown to play an important role in regulating the expression of Kv4.2 in diabetes [56] and controlling autoimmune demyelination by regulating the T-helper 17 immune response [57]. [score:5]
miR-301a binds the predicted 3′UTR target sites of PTEN and reduces PTEN expression. [score:5]
a, The predicted miR-301a target sequence in the 3′UTR target sites of the PTEN gene. [score:5]
antagomir control, ANOVA test) We next tested whether miR-301a mediates glycine -induced neuroprotection through PTEN down-regulation. [score:4]
We demonstrated that PTEN down-regulation by PTEN siRNA prevented miR-301a antagomir from blocking glycine -induced neuroprotection (Fig.   8c). [score:4]
These data indicate that miR-301 negatively regulates the mRNA and protein expression of PTEN in cortical neurons. [score:4]
The mutation of the seed sequence of miR-301a within the 3′UTR of PTEN abrogated the inhibition of luciferase activity by exogenous miR-301a agomir in PC12 cells (Fig.   6b). [score:4]
Interestingly, we reveal that glycine acts as an upstream regulator to enhance miR-301a expression, which confer neuroprotection in cortical neurons. [score:4]
miR-301a is also up-regulated in gastric tumor cells and involved in the clinical progression and prognosis of gastric cancer [45]. [score:4]
These results suggest that miR-301a directly binds the predicted 3′UTR target sites of PTEN. [score:4]
To determine whether miR-301a directly binds the predicted 3′UTR sites of PTEN, we made a reporter construct harbouring the 589 bp fragment of PTEN 3′UTR flanking the entire putative target sequence. [score:4]
We revealed that PTEN down-regulation by microRNA-301a mediated glycine -induced neuroprotective effect following oxygen-glucose deprivation. [score:4]
Control: untransfected PC12 cells; Blank: PC12 cells transfected with pMIR-REPORT Luciferase vector carrying PTEN wild-type or PTEN mutant without miR-301a agomir or antagomir To determine the functional consequence of miR-301a binding to PTEN, we tested the effects of miR-301a agomir or antagomir on the mRNA and protein expression of PTEN in cortical neurons. [score:3]
a, Glycine treatment increases miR-301a expression after OGD (n = 3, * P < 0.05 vs. [score:3]
We examined the expression of miR-301a in cultured cortical neurons at different time after OGD insult. [score:3]
PTEN is a target gene of miR-301a. [score:3]
We showed that suppression of miR-301a by miR-301a antagomir attenuated glycine -induced neuroprotective effect (Fig.   5b). [score:3]
Our study for the first time demonstrates that miR-301a exerts a neuroprotective effect in OGD -induced neuronal injury, implicating a therapeutic potential of miR-301a signaling in neurological diseases. [score:3]
The levels of miR-301a detected by microarray were normalized to a negative control of U6 snRNA To provide further evidence to verify glycine -induced increase of miR-301a, qRT-PCR was used to measure the miR-301a expression after the rat cortical neurons were treated with glycine (100 μM) for 24 h. As expected, the qRT-PCR results confirmed that glycine enhanced the expression of miR-301a in the cortical neurons (Fig.   3). [score:3]
Taken together, we conclude that miR-301a targets PTEN to mediate glycine -induced neuroprotection. [score:3]
qRT-PCR reveals that treatment of glycine (100 μM) for 24 h increased the expression of miR-301a in cultured cortical neurons (n = 6, * P < 0.05 vs. [score:3]
Inj, injury; Gly, glycine; Ant, antagomir; Ant-con, antagomir control; Ago, agomir; Ago-con, agomir control To explore how miR-301a exerts its effect in mediating glycine -induced neuroprotection, we analyzed the target genes of miR-301a by miRanda (www. [score:3]
miR-301a promotes migration and invasion by targeting TGFBR2 in human colorectal cancer [48]. [score:3]
Glycine increases miR-301a expression in cortical neurons. [score:3]
miR-301a contributes to IL-6 -induced insulin resistance by direct regulation of PTEN and downstream Akt signaling [47]. [score:3]
Collectively, these data indicate that glycine confers neuroprotection through enhancing miR-301a expression. [score:3]
Recent studies demonstrate that miR-301a promotes cancer cell metastasis in breast, hepatocellular and gastric tumors through different target genes [43, 44, 48]. [score:3]
Western blot analysis further showed that 24 h treatment of miR-301 agomir decreased the protein expression of PTEN but 24 h treatment of miR-301 antagomir increased the level of PTEN proteins in cultured cortical neurons (Fig.   7b-c). [score:3]
Fig. 2Glycine -induced increase of miR-301a expression in cortical neurons by microarray analysis. [score:3]
org) and predicted PTEN as a target of miR-301a. [score:3]
The levels of miR-301a detected by microarray were normalized to a negative control of U6 snRNATo provide further evidence to verify glycine -induced increase of miR-301a, qRT-PCR was used to measure the miR-301a expression after the rat cortical neurons were treated with glycine (100 μM) for 24 h. As expected, the qRT-PCR results confirmed that glycine enhanced the expression of miR-301a in the cortical neurons (Fig.   3). [score:3]
miR-301a, microRNA-301a; OGD, oxygen-glucose deprivation; PTEN, phosphatase and tensin homolog deleted on chromosome 10; 3′UTR, 3′-untranslated region; LDH, lactate dehydrogenase; MTT, thiazolyl blue tetrazolium bromide; FDA, fluorescein diacetate Not applicable. [score:3]
We found that glycine treatment resulted in differential changes in the expression of miRNAs in the cortical neurons (Fig.   2a), among which the miR-301a was markedly increased (Fig.   2b). [score:3]
miR-301a suppresses PTEN to mediate glycine -induced neuroprotection. [score:3]
We show that the expression of miR-301a is elevated by glycine. [score:3]
The qRT-PCR data revealed that the expression of miR-301a, but not miR-146a, was decreased at 2, 6, 12 and 24 h after OGD -induced injury in cultured cortical neurons (Fig.   4a, b). [score:3]
As shown in Fig.   6a, miR-301a was predicted to target the 2206–2212 nts of PTEN 3′UTR. [score:3]
We provide evidence that glycine is an upstream regulator of microRNA-301a. [score:2]
b, The data of microarray assay show that the expression of miR-301a is remarkably increased in glycine (100 μM) -treated cortical neurons (n = 3, * P < 0.05 vs. [score:2]
We would reason that glycine may regulate miR301a through a transcriptional mechanism by which Dicer is modulated. [score:2]
We performed luciferase assay and showed that ectopic expression of miR-301a agomir resulted in a significant reduction of luciferase activity in the PC12 cells (Fig.   6b). [score:2]
As glycine is a co-agonist of NMDA receptors, regulation of miR301a by glycine may be mediated by NMDA receptor -dependent signaling. [score:2]
It is not yet clear how miR301a is regulated by glycine. [score:2]
miR-301a has been shown to involve in some biological and pathological processes, including cell development, cell differentiation, inflammation, apoptosis and cancer [42– 45]. [score:2]
Our results suggest that 1) microRNA-301a is neuroprotective in oxygen-glucose deprivation -induced neuronal injury; 2) glycine is an upstream regulator of microRNA-301a; 3) glycine confers neuroprotection through microRNA-301a/PTEN signal pathway. [score:2]
The levels of miRNAs were calculated using U6 snRNA as an internal control Given the neuroprotective effect of glycine, the observed up-regulation of miR-301a by glycine led us to reason that miR-301a may play a neuroprotective role in neuronal injury. [score:2]
Thus, we identify a molecular mechanism by which the glycine/miR-301a signal pathway negatively regulates PTEN in conferring neuroprotection. [score:2]
PTEN is regulated by miR-301a in cortical neurons. [score:2]
Through negative regulation of SMAD4, miR-301a promotes pancreatic cancer progression [55]. [score:2]
Kawano M, Tanaka K, Itonaga I, Iwasaki T, Tsumura H. MicroRNA-301a promotes cell proliferation via PTEN targeting in Ewing’s sarcoma cells. [score:2]
a, The expression of miR-301a in cultured cortical neurons at different time following OGD insult are measured by qRT-PCR. [score:1]
Fig. 3Verification of glycine -induced increase of miR-301a by qRT-PCR. [score:1]
miR-301a antagomir control, ANOVA test). [score:1]
The data are normalized to that in Sham 1. c, Treatment of miR-301a agomir reduces OGD -induced cortical neuronal death. [score:1]
We conclude that glycine confers neuroprotection through microRNA-301a/PTEN signal pathway. [score:1]
Site-directed mutagenesis was performed to disrupt the sequence within PTEN mRNA-3′UTR which was complementary to the miR-301a (MIMAT0000552) seed region, and the primers were purchased from RioBio (China). [score:1]
MiRNA-301a (miR-301a) is the member of miR-130/301a family. [score:1]
b, Treatment of miR-301a antagomir, but not antagomir control, attenuates glycine -induced neuroprotection against LDH release in cultured cortical neurons subjected to OGD insult. [score:1]
At 24 h after OGD insult, we showed that the neuroprotective efficiency induced by glycine in agomir -treated neurons was not significantly higher than that in agomir control -treated neurons (Fig.   5c), suggesting that miR-301a is in the same pathway with glycine to exert neuroprotective effect. [score:1]
To provide further evidence, we treated the neurons with miR-301a agomir or agomir control. [score:1]
At 24 h after the transduction, the neurons were treated with miR-301a antagomir or antagomir control. [score:1]
The cortical neurons were then treated with lentiviral PTEN siRNA or miR-301a antagomir. [score:1]
c, Treatment of miR-301a agomir in cultured cortical neurons does not enhance glycine -induced neuroprotective effect after OGD insult. [score:1]
miR-301a is decreased at 2, 6, 12 & 24 h after OGD insult (n = 3, * P < 0.05 vs. [score:1]
In the present study, we demonstrate that glycine -induced neuroprotection depends on miR-301a and its downstream signaling. [score:1]
But it is not known whether microRNA-301a has a neuroprotective property. [score:1]
The luciferase activity was increased in the PC12 cells co -transfected with a luciferase reporter containing the pMIR-PTEN 3′UTR and miR-301a antagomir (n = 6, * P < 0.05 vs. [score:1]
c, PTEN siRNA treatment prevents miR-301a antagomir from blocking glycine -induced neuroprotection. [score:1]
miR-301a Glycine PTEN Neuroprotection Glycine is the simplest non-essential amino acid, which is a critical building block in many proteins. [score:1]
Inj, injury; Gly, glycine; Ant, antagomir; Ant-con, antagomir control; Ago, agomir; Ago-con, agomir controlTo determine whether miR-301a is neuroprotective, the cortical neurons were treated with miR-301a agomir or agomir control. [score:1]
miR-301a mediates glycine -induced neuroprotective effect in cultured cortical neurons subjected to oxygen-glucose deprivation (OGD). [score:1]
Inj, injury; Gly, glycine; Ant, antagomir; Ant-con, antagomir control; Ago, agomir; Ago-con, agomir control To determine whether miR-301a is neuroprotective, the cortical neurons were treated with miR-301a agomir or agomir control. [score:1]
At 24 h after the treatment, the neurons were subjected to OGD for 1 h. At 24 h after OGD insult, we found that treatment of miR-301a agomir, but not the agomir control, protected against OGD -induced neuronal death after OGD insult (Fig.   4c). [score:1]
miR-301a is required for glycine -induced neuroprotection. [score:1]
To provide evidence whether glycine -induced increase of miR-301a conferred neuroprotection, the cortical neurons were treated with miR-301a antagomir or antagomir control. [score:1]
d, Treatment of miR-301a antagomir increases OGD -induced neuronal death. [score:1]
Recent studies indicate that miR-301a plays a critical role in tumorigenesis [43, 44, 46, 48]. [score:1]
In contrast, the luciferase activity was increased in the PC12 cells co -transfected with a luciferase reporter containing the PTEN-3′UTR (pMIR-PTEN 3′UTR) and miR-301a antagomir (Fig.   6c). [score:1]
The microRNA-301a is involved in both biological and pathological processes. [score:1]
Our results indicate that microRNA-301a is neuroprotective in oxygen-glucose deprivation -induced neuronal injury. [score:1]
miR-301a agomir control, ANOVA test). [score:1]
In the same experimental protocols, treatment of miR-301a antagomir but not antagomir control increased OGD -induced neuronal death (Fig.   4d). [score:1]
These results provides the first evidence that miR-301a is neuroprotective in neuronal injury. [score:1]
However, it is not clear whether miR-301a plays a role in neuronal survival. [score:1]
miR-301a is neuroprotective in OGD -induced neuronal injury. [score:1]
To determine whether glycine -induced neuroprotection is mediated through miR-301a, we first measured the effects of glycine on the expression of miR-301a in cultured cortical neurons at different time following OGD insult. [score:1]
The qRT-PCR data showed that glycine prevented OGD -induced decrease of miR-301a at 2, 6, 12 and 24 h after injury in cultured cortical neurons (Fig.   5a). [score:1]
In this study, we aimed to determine whether glycine -induced neuroprotection requires microRNA-301a -dependent signaling. [score:1]
The luciferase activity was reduced in the PC12 cells co -transfected with a luciferase reporter containing the PTEN 3′UTR and miR-301a agomir (n = 6, * P < 0.05 vs. [score:1]
The miR-301a agomir, agomir control, antagomir, antagomir control were purchased from RioBio (China). [score:1]
A total of 5 × 10 [4] PC12 cells were seeded in 24-well plates for 24 h and then co -transfected with 100 ng pMIR-PTEN-3′UTR constructs using Lipofectamine 2000 (Invitrogen, USA) with 1.0 μM miR-301a agomir or agomir control, or with the miR-301a antagomir or antagomir control. [score:1]
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[+] score: 131
Hypoxia led to p38 and JNK phosphorylation, which was inhibited by miRNA-301a overexpression, and miRNA-301a inhibitor treatment interrupted the inhibitory effect of miRNA-301a on p38 and JNK phosphorylation (Figure 4B). [score:9]
Hypoxia consistently caused increased ASK1 mRNA and protein expression levels, as shown in Figure 1, whereas miRNA-301a mimic treatment caused decreases in ASK protein expression and phosphorylation as well as ASK1 mRNA expression. [score:7]
To determine whether miRNA-301a regulates cell survival by targeting ASK1 under hypoxic conditions, cell viability was examined under hypoxic conditions, followed by treatment with a miR-301a mimic or inhibitor. [score:6]
In our study, as miRNA-301a expressed by stem cells could be released into the adjacent environment, which includes other cell types, determining the effect of miRNA-301a on regulating ASK1 expression in other cardiac cell types is important. [score:6]
To investigate the signaling molecules that are regulated by miRNA-301a, which target ASK1 under hypoxic conditions, we first examined the ASK1 mRNA and protein expression levels under hypoxic conditions with or without miRNA-301a overexpression. [score:6]
We used a miRNA that targets ASK1 as a regulatory tool to modulate ASK1 expression and stem cell activation under hypoxic conditions and investigated the regulatory effect of miRNA-301a on ASK1 -mediated apoptosis in hASCs. [score:5]
In this study, we investigated the overexpression of miRNA-301a in human ASCs (hASCs) and found that this miRNA increased cell survival by inhibiting ASK1 expression under hypoxic conditions. [score:5]
We also observed that the expression level of ASK1 was associated with cell death, and that miRNA-301a overexpression could attenuate the activation of hypoxia -induced apoptotic signaling in hASCs. [score:5]
Our data indicated that miRNA-301a suppressed the hypoxia -induced expression and activation of proapoptosis-related factors (JNK, p38, and NFκB). [score:5]
miRNA-301a mimic treatment showed a significant protective effect against cell death, but a miRNA-301a inhibitor blocked the protective effect of miRNA-301a overexpression (Figure 3A). [score:5]
Considering these findings, we speculate that controversial effects may not occur among different cell types, and we anticipate a consistent effect of miRNA-301a regulation of ASK1 expression and activation on hASCs [miR-301] transplanted into infarcted hearts. [score:4]
2.4. miRNA-301a Represses the Apoptotic Pathway via Down-Regulation of the ASK1-Mediated Signaling Pathway during Hypoxia. [score:4]
To determine whether miRNA-301a regulates the ASK1 -mediated apoptotic pathway, we examined JNK and p38 activation under hypoxic conditions with or without miRNA-301a overexpression. [score:4]
Moreover, the regulation of ASK1 expression and activation by miRNA-301a considerably improved stem cell survival and increased ischemic heart function (Figure 5). [score:4]
As an apoptosis -associated transcription factor, NFκB was investigated to determine the anti-apoptotic effect of ASK1 inhibition by miRNA-301a overexpression. [score:3]
Mature miRNA-301a mimics (Genolution Pharmaceuticals, Seoul, Korea) and miRNA-301a inhibitors (Integrated DNA Technologies, Coralville, IA, USA) were used at final concentrations of 50 nM. [score:3]
Hypoxic stress resulted in NFκB phosphorylation, whereas miRNA-301a mimic treatment attenuated NFκB phosphorylation; this effect was reversed by miRNA-301a inhibitor treatment (Figure 4B). [score:3]
miRNA-301a was not able to inhibit caspase 3 activation (Figure S6). [score:3]
Therefore, we further examined caspase 3 activation to determine whether miRNA-301a inhibits the mitochondrial -dependent apoptosis mediated by ASK1. [score:3]
The threshold cycle (C [t]) of miR-301a and U6 expression was automatically defined, located in the linear amplification phase of the PCR, and normalized to the control U6 (Δ C [t] value). [score:3]
Additionally, these effects were reversed by miR-301a inhibitor treatment of these cells (Figure 4A,B). [score:3]
We investigated the protective effects of ASK1 inhibition by candidate miRNA transfection on cell death under hypoxic conditions, and we found that around eight miRNAs, including miR-301a overexpression, showed the protective effect against cell death (Figure S2). [score:3]
In addition, we confirmed that endogenous miR-301a expression decreased until 24 h in hASCs under hypoxic conditions (Figure 2D). [score:3]
Patel N. Tahara S. M. Malik P. Kalra V. K. Involvement of mir-30c and mir-301a in immediate induction of plasminogen activator inhibitor-1 by placental growth factor in human pulmonary endothelial cells Biochem. [score:3]
Although we did not investigate these proteins which can support ASK1 function in the present study, miRNA-301a inhibited ASK1 phosphorylation through transcriptional and translational repression of ASK1, resulting in the attenuation of cell death (Figure 3 and Figure 4). [score:3]
2.2. miRNA-301a Targeted ASK1 in hASCs. [score:3]
This study is the first demonstration of ASK1 modulation using a miRNA in transplanted stem cells in a MI mo del and suggests that the suppression of ASK1 by miRNA-301a is a promising approach to prevent massive death of stem cells after transplantation. [score:3]
Then, we used an annexin V assay to test the anti-apoptotic effect of miRNA-301a under hypoxic conditions and confirmed the anti-apoptotic effect of ASK1 inhibition using miRNA-301a under hypoxic conditions (Figure 3B and Figure S4). [score:2]
Luciferase assay using vectors containing the 3′ UTR of ASK1 confirmed that miRNA-301a targets ASK1 (Figure 2C). [score:2]
Additionally, miRNA-301a treatment was capable of attenuating hASCs apoptosis by regulating cytosolic in hypoxia -treated cells and in a MI heart. [score:2]
2.3. miRNA-301a Has Anti-Apoptotic Effects on hASCs under Hypoxic Conditions. [score:1]
To determine whether miRNA-301a -transfected hASCs (hASCs [miR-301]) have a therapeutic effect on ischemic myocardium, cardiac functional improvements by hASCs [miR-301] were analyzed in normal and MI rat hearts after hASC [miR-301] transplantation. [score:1]
The relative difference in the expression level of miR-301a in the sorted cells (ΔΔ C [t]) was calculated and presented as the fold induction (2–ΔΔ Ct). [score:1]
Although few studies have reported on an association between miRNA-301a and ASK1 in cardiomyocytes, the role of ASK1 in apoptosis has been well established. [score:1]
Figure 5C shows that transplanted hASCs [miR-301] had greater survivorship rates than transplanted hASCs at injected sites, with less cell death observed in hASCs [miR-301] injected heart tissue (Figure 5D). [score:1]
The fibrosis area was significantly reduced by hASCs [miR-301] injection in ischemic hearts (Figure 5B). [score:1]
miRNA-301a was also reported to be related to vascular dysfunction in human pulmonary endothelial cells [35]. [score:1]
Effect of hASC [miR-301] on Ischemic MyocardiumTo determine whether miRNA-301a -transfected hASCs (hASCs [miR-301]) have a therapeutic effect on ischemic myocardium, cardiac functional improvements by hASCs [miR-301] were analyzed in normal and MI rat hearts after hASC [miR-301] transplantation. [score:1]
Effect of hASC [miR-301] on Ischemic Myocardium. [score:1]
We found that the miRNA-301a binding site is highly conserved in the 3′ UTR of ASK1 mRNA. [score:1]
In addition, we further investigated the protective effect using siRNA for ASK1 under hypoxic conditions, as ASK1 is one of the major targets of miRNA-301a (Figure S3). [score:1]
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4
[+] score: 29
The results of luc reporter assays are summarized in Figure 10, C and D. The data showed that miR-143 and miR-155 down-regulated the WT2 c-Maf 3′-UTR, and miR-301a down-regulated the WT3 c-Maf 3′-UTR (Figure 10C, n = 6, P < 0.05). [score:6]
To determine whether the aforementioned miRNAs identified in rat lens explant system are also expressed during mammalian lens development in vivo, we conducted ISH analysis of miR-9, miR-143, miR-155, miR-301a, miR-381, and miR-455 in E14.5 and newborn (P0) lenses. [score:4]
The current data suggest that multiple miRNAs, including miR-9, miR-137, miR-155, miR-301a, miR455, and miR-543 (Figure 7A and Figure 8A), regulate c-Maf expression through its 3′-UTR. [score:4]
Expression of the lens-differentiation factor c-Maf was predicted to be regulated by multiple miRNAs and experimentally validated for three miRNAs, including miR-143, miR-155, and miR-301a, in lens cells. [score:4]
Taken together, the present data demonstrate that miR-143 and miR-301a are novel regulatory miRNAs for c-Maf expression in mammalian lens. [score:4]
The miR-143, miR-155, and miR-301a down-regulated expression of c-Maf evaluated in cultured lens cells through the 3′-UTR luciferase reporter assays. [score:3]
Similar analysis of “late” group, including c-Maf, Ets1, N-Myc, Nfat5, and Nfib, yielded 10 miRNAs: miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351, with multiple connections. [score:1]
Note for miR-301a (E), a weak staining is detectable in these structures at E14.5. [score:1]
At postnatal day P0, the distribution of both miR-9 (B) and miR-143 (D) is largely maintained in all the lens cells previously described for the E14.5 lens, whereas miR-301a (F) is not detected. [score:1]
Ten miRNAs, miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351. [score:1]
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[+] score: 16
Loss of function approach in in vitro mo del (H9C2 cells) using miR-301a inhibitor was used to test if the increase in miR-301 has a role in regulation of Kv4.2 gene expression, a voltage-gated K [+] channel. [score:6]
Specifically, mir-301 and mir-17-5p showed different expression levels after occlusion, while mir-301 expression decreased, we observed an increased in mir-17-5p expression compared to control. [score:6]
We observed a decreased miR-301 and miR-93 expressions in occlusion group compared to ablation. [score:2]
Panguluri et al. (2013) identified a significant elevation of miR-301a as a key modulator in diabetic condition. [score:1]
MicroRNA-301a mediated regulation of Kv4.2 in diabetes: identification of key modulators. [score:1]
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[+] score: 15
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-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, 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]
Of these miRNAs, 12 were upregulated (miR-34b, miR-138, miR-297a, miR-301, miR-449, miR-466, miR-493, miR-579, miR-582, miR. [score:4]
Three dysregulated miRNAs (miR-301, miR-369, and miR-669k) overlapped in the lungs of adenoma-bearing mice and of microadenoma-bearing mice. [score:2]
These miRNAs were miR-301, miR-369, and miR-669k, whose main functions are to regulate cell proliferation, autophagy, and aerobic glycolysis, which are mechanisms involved in the initial stage of the functional transformation of cells into their neoplastic counterpart. [score:2]
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[+] score: 7
Seven overexpressed miRNAs (miR-20a, miR-199a-5p, miR-199, miR-323, miR-301a, miR-301b and miR-130b) showed the most target mRNAs. [score:5]
The miRNAs including miR-301a, miR-301b and miR-130b regulated some important genes, including TGF-βR1, TGF-βR2, Smad2, Smad4 and Smad5 and, therefore, might be of great importance to the activation of the organ of Corti. [score:2]
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[+] score: 4
There are 6 common miRNAs (miR-138, miR-301a, miR-33, miR-34a, miR-146a, and miR-23a) between our data set and work of Hu et al. who studied miRNA expression profiles in a pilocarpine -induced mo del of epilepsy [23]. [score:3]
Additionally, four miRNAs (miR-138, miR-146b, miR-301a, and miR-92b) were common between our data and those of Kan et al. in human temporal lobe epilepsy [22]. [score:1]
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[+] score: 4
Recent studies revealed that miR-19b, miR-30a, miR-301a promoted the progression of periodontitis [4] and miR-146a, miR-98 were upregulated to contribute to the progression of OA [10]. [score:4]
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[+] score: 2
Some deregulated miRNAs were identified both in the TLE patients of Kan’s work and in our rat TLE mo del, such as miR-27a, miR-190, miR-203 and miR-301a. [score:2]
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[+] score: 2
Namely, pregnant rats fed SO and FO diets during the first 12 days of pregnancy showed significant lower expression of miR-449c-5p, miR-134–5p, miR-188, miR-32, miR130a, miR-144–3p, miR-431, miR-142–5p, miR-33, miR-340–5p, miR-301a, miR-30a, miR-106b, and miR-136–5p, as compared with OO, LO, and PO diets. [score:2]
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12
[+] score: 2
Other miRNAs from this paper: hsa-mir-301a
Zhang W Zhang T Jin R Zhao H Hu J Feng B MicroRNA-301a promotes migration and invasion by targeting TGFBR2 in human colorectal cancerJ Exp Clin Cancer Res. [score:2]
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