Effect of Y Doping on Superconductivity and Spin-Density-Wave States in Sm1−x Y x FeAsO0.8F0.2 and Sm1−x Y x FeAsO

Chen, Y. L.; Cui, Yun; Cheng, C.H.; Yang, Ye; Zhang, Y.; Zhao, Yong

doi:10.1007/s10948-010-0698-8

Cited by 60 publications

(77 citation statements)

References 9 publications

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“…In addition, one group of miRNAs were isolated from rat left ventricles at 6 h after IP. Each group had six rats, and miRNA expression profiling was done by miRNA microarray analysis using a chip containing 341 mature miRNAs (Chip ID miRRat 12.0 version; LC Sciences) (24,25). The miRNA expression was demonstrated by the mean of the 6 biological replicates.…”

Section: Methodsmentioning

confidence: 99%

“…Hypoxia was achieved by placing the cells in a hypoxia chamber filled with 5% CO 2 and 95% N 2 at 37°C for 4 h. Following hypoxia exposure, the cells were reoxygenated with 5% CO 2 (24,25). For the miR-21 knockdown, miR-21 inhibitor (LNA-anti-miR-21) (Exiqon, Inc.) was added to the culture medium at a final oligonucleotide concentration of 30 nM.…”

Section: Construction Of the Adenovirus Expressing Mir-21 Programmedmentioning

confidence: 99%

See 1 more Smart Citation

MicroRNA Expression Signature and the Role of MicroRNA-21 in the Early Phase of Acute Myocardial Infarction

Dong¹,

Cheng²,

Yang³

et al. 2009

Journal of Biological Chemistry

415

402

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Several recent reports have suggested that microRNAs (miRNAs) might play critical roles in acute myocardial infarction (AMI). However, the miRNA expression signature in the early phase of AMI has not been identified. In this study, the miRNA expression signature was investigated in rat hearts 6 h after AMI. Compared with the expression signature in the noninfarcted areas, 38 miRNAs were differentially expressed in infarcted areas and 33 miRNAs were aberrantly expressed in the border areas. Remarkably, miR-21 expression was significantly down-regulated in infarcted areas, but was up-regulated in border areas. The down-regulation of miR-21 in the infarcted areas was inhibited by ischemic preconditioning, a known cardiac protective method. Overexpression of miR-21 via adenovirus expressing miR-21 (Ad-miR-21) decreased myocardial infarct size by 29% at 24 h and decreased the dimension of left ventricles at 2 weeks after AMI. Using both gain-of-function and loss-offunction approaches in cultured cardiac myocytes, we identified that miR-21 had a protective effect on ischemia-induced cell apoptosis that was associated with its target gene programmed cell death 4 and activator protein 1 pathway. The protective effect of miR-21 against ischemia-induced cardiac myocyte damage was further confirmed in vivo by decreased cell apoptosis in the border and infarcted areas of the infarcted rat hearts after treatment with Ad-miR-21. The results suggest that miRNAs such as miR-21 may play critical roles in the early phase of AMI. MicroRNAs (miRNAs)3 are endogenous, noncoding, singlestranded RNAs of ϳ22 nucleotides and constitute a novel class of gene regulators (1-3). Analogous to the first RNA revolution in the 1980s, when Zaug and Cech (4) discovered the enzymatic activity of RNA, the more recent discoveries of RNA interference and miRNA may represent the second RNA revolution (5).Although the first miRNA, lin-4, was discovered in 1993 (6, 7), their presence in vertebrates was confirmed only in 2001 (8). miRNAs are initially transcribed in the nucleus by RNA polymerase II or III to form large pri-miRNA transcripts (9). These pri-miRNAs are then processed by the RNase III enzymes, Drosha, Pasha, and Dicer, to generate 18-to 24-nucleotide mature miRNAs. In addition to this miRNA biogenesis pathway, some miRNA precursors are able to bypass Drosha processing to produce miRNAs via Dicer, possibly representing an alternative pathway for miRNA biogenesis (10, 11). The mature miRNAs bind to the 3Ј-untranslated region of their mRNA targets and negatively regulate gene expression via degradation or translational inhibition.Currently, about 600 miRNAs have been cloned and sequenced in humans, and the estimated number of miRNA genes is as high as 1,000 in the human genome (12, 13). Functionally, an individual miRNA is as important as a transcription factor because it is able to regulate the expression of its multiple target genes. As a group, miRNAs are estimated to regulate over 30% of the genes in a cell (14). It is thus not surprising th...

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Section: Methodsmentioning

confidence: 99%

Section: Construction Of the Adenovirus Expressing Mir-21 Programmedmentioning

confidence: 99%

MicroRNA Expression Signature and the Role of MicroRNA-21 in the Early Phase of Acute Myocardial Infarction

Dong¹,

Cheng²,

Yang³

et al. 2009

Journal of Biological Chemistry

415

402

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“…In order to adjust the notation in Eqs. (14), (15), (17), and (18) to those given in the appendix, one has to replace q 1 ↔ q 2 in Eqs. (15) and (17) and then introduce the dimensionless form factors A 1 = A/m and A 2 = ±m B (p 2 = m 2 ) where the sign "+ ′′ stands for Eqs.…”

mentioning

confidence: 99%

Four-quark structure of the Zc(3900) , Z(4430) , and
Fabian
¹
,
Gutsche
²
,
Ivanov
³

et al. 2016
Phys. Rev. D

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“…Similarly, Roy et al (14) show that miR-21 is elevated in the myofibroblast-infiltrated area 7 days after ischemia/ reperfusion and suppresses metalloprotease-2 via targeting PTEN. More recently, studies have shown that miR-21 exerts an antiapoptotic function in cardiac myocytes via inhibiting PDCD4 (15) and reduces infarct size via local viral delivery to the heart (16). However, the signaling pathway that regulates miR-21 has not been identified.…”

mentioning

confidence: 99%

MicroRNA-21 Is a Downstream Effector of AKT That Mediates Its Antiapoptotic Effects via Suppression of Fas Ligand

Sayed¹,

He²,

Hong³

et al. 2010

Journal of Biological Chemistry

287

213

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MicroRNA-21 (miR-21) is highly up-regulated during hypertrophic and cancerous cell growth. In contrast, we found that it declines in cardiac myocytes upon exposure to hypoxia. Thus, the objective was to explore its role during hypoxia. We show that miR-21 not only regulates phosphatase and tensin homologue deleted on chromosome 10 (PTEN), but also targets Fas ligand (FasL). During prolonged hypoxia, down-regulation of miR-21 proved necessary and sufficient for enhancing expression of both proteins. We demonstrate here for the first time that miR-21 is positively regulated via an AKT-dependent pathway, which is depressed during prolonged hypoxia. Accordingly, hypoxia-induced down-regulation of miR-21 and up-regulation of FasL and PTEN were reversed by activated AKT and reproduced by a dominant negative mutant, wortmannin, or PTEN. Moreover, the antiapoptotic function of AKT partly required miR-21, which was sufficient for inhibition of caspase-8 activity and mitochondrial damage. In consensus, overexpression of miR-21 in a transgenic mouse heart resulted in suppression of ischemia-induced up-regulation of PTEN and FasL expression, an increase in phospho-AKT, a smaller infarct size, and ameliorated heart failure. Thus, we have identified a unique aspect of the function of AKT by which it inhibits apoptosis through miR-21-dependent suppression of FasL. MicroRNA (miRNA)3 are molecules approximately twenty ribonucleotides long that specifically target mRNA through partial complementarity and, thereby, inhibit translation and/or induce their degradation. miR-21 is one of the most commonly and dramatically up-regulated miRNA in many cancers (1, 2) and has been implicated in the inhibition of programmed cell death (2). Some of its validated targets include tropomyosin 1 (3), PTEN (2, 4, 5), programmed cell death 4 (Pdcd4) (6, 7), TAp63 isoform of p53 family, and LRRFIP1, an inhibitor of NFB signaling (8). Similarly, miR-21 is one of the most highly and consistently up-regulated miRNA during cardiac hypertrophy (9 -12). Thum et al. (13) show that miR-21 is predominantly up-regulated in the myofibroblasts where it targets sprouty1 and enhances their survival and, thereby, fibrosis in the heart. Similarly, Roy et al. (14) show that miR-21 is elevated in the myofibroblast-infiltrated area 7 days after ischemia/ reperfusion and suppresses metalloprotease-2 via targeting PTEN. More recently, studies have shown that miR-21 exerts an antiapoptotic function in cardiac myocytes via inhibiting PDCD4 (15) and reduces infarct size via local viral delivery to the heart (16). However, the signaling pathway that regulates miR-21 has not been identified.Two of the molecules that play a major role in ischemic injury of the heart include PTEN and FasL. PTEN is a major negative regulator of AKT (17) whose activity is modulated by its abundance, oxidation, or phosphorylation (18). It is also targeted by miR-21, which provides a specific post-transcriptional mechanism for regulating its expression (2, 4, 5). PTEN has been regarded as the A...

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Effect of Y Doping on Superconductivity and Spin-Density-Wave States in Sm1−x Y x FeAsO0.8F0.2 and Sm1−x Y x FeAsO

Cited by 60 publications

References 9 publications

MicroRNA Expression Signature and the Role of MicroRNA-21 in the Early Phase of Acute Myocardial Infarction

MicroRNA Expression Signature and the Role of MicroRNA-21 in the Early Phase of Acute Myocardial Infarction

Four-quark structure of the Zc(3900) , Z(4430) , and
Fabian
¹
,
Gutsche
²
,
Ivanov
³

et al. 2016
Phys. Rev. D

MicroRNA-21 Is a Downstream Effector of AKT That Mediates Its Antiapoptotic Effects via Suppression of Fas Ligand

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Effect of Y Doping on Superconductivity and Spin-Density-Wave States in Sm1−x Y x FeAsO0.8F0.2 and Sm1−x Y x FeAsO

Cited by 60 publications

References 9 publications

MicroRNA Expression Signature and the Role of MicroRNA-21 in the Early Phase of Acute Myocardial Infarction

MicroRNA Expression Signature and the Role of MicroRNA-21 in the Early Phase of Acute Myocardial Infarction

Four-quark structure of the Zc(3900) , Z(4430) , and Fabian1, Gutsche2, Ivanov3 et al. 2016Phys. Rev. D

MicroRNA-21 Is a Downstream Effector of AKT That Mediates Its Antiapoptotic Effects via Suppression of Fas Ligand

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Product

Resources

About

Four-quark structure of the Zc(3900) , Z(4430) , and
Fabian
¹
,
Gutsche
²
,
Ivanov
³

et al. 2016
Phys. Rev. D