miR‐17, miR‐19b, miR‐20a, and miR‐106a are down‐regulated in human aging

Hackl, Matthias; Brunner, Stefan M.; Fortschegger, Klaus; Schreiner, Carina; Mičutková, Lucia; Mück, Christoph; Laschober, Gerhard; Lepperdinger, Günter; Sampson, Natalie; Berger, Peter; Herndler‐Brandstetter, Dietmar; Wieser, Matthias; Kühnel, Harald; Strasser, Alois; Rinnerthaler, Mark; Breitenbach, Michael; Mildner, Michael; Eckhart, Leopold; Tschachler, Erwin; Trost, Andrea; Bauer, Johann; Papak, Christine; Trajanoski, Zlatko; Scheideler, Marcel; Grillari‐Voglauer, Regina; Grubeck‐Loebenstein, Beatrix; Jansen‐Dürr, Pidder; Grillari, Johannes

doi:10.1111/j.1474-9726.2010.00549.x

Cited by 325 publications

(268 citation statements)

References 55 publications

(71 reference statements)

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“…Our data correlated with those of previous reports on trabecular meshwork cells and human foreskin fibroblasts (BJ) Bonifacio and Jarstfer 2010;Christoffersen et al 2010;Bhaumik et al 2009). However, previous data on miR-146a expression in HUVECs during replicative senescence showed conflicting results (Hackl et al 2010;Vasa-Nicotera et al 2011). In particular, Hackl et al (2010) reported no significant change of miR-146a expression in senescent HUVECs, whereas Vasa-Nicotera et al (2011) observed a significant decrease of miR-146a expression in senescent cells.…”

Section: Discussionmentioning

confidence: 97%

“…However, previous data on miR-146a expression in HUVECs during replicative senescence showed conflicting results (Hackl et al 2010;Vasa-Nicotera et al 2011). In particular, Hackl et al (2010) reported no significant change of miR-146a expression in senescent HUVECs, whereas Vasa-Nicotera et al (2011) observed a significant decrease of miR-146a expression in senescent cells. Interestingly, we found an up-regulation of miR-146a expression not only in HUVECs, but also in HAEC and in HCAEC senescent cells, confirming that its up-regulation is associated with senescent phenotype in different vascular cell types.…”

Section: Discussionmentioning

confidence: 97%

“…Human umbilical vein endothelial cells (HUVECs) have been extensively used as an in vitro endothelial model representing common functional and morphological features of the in vivo endothelial cells (Unterluggauer et al 2007). This model was recently used to identify miRs and their relative target proteins associated with replicative and/or stress-induced senescence (Ito et al 2010;Menghini et al 2009;Hackl et al 2010;Vasa-Nicotera et al 2011;Magenta et al 2011). However, these recent reports have not been conclusive on identifying specific miRs as markers of vascular ageing-associated dysfunction in vivo.…”

Section: Introductionmentioning

confidence: 99%

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MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling

Olivieri

Lazzarini

Recchioni

et al. 2012

AGE

176

154

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In order to identify new markers of vascular cell senescence with potential in vivo implications, primary cultured endothelial cells, including human umbilical vein endothelial cells (HUVECs), human aortic endothelial cells (HAECs), human coronary artery endothelial cells (HCAECs) and ex vivo circulating angiogenic cells (CACs), were analysed for microRNA (miR) expression. Among the 367 profiled miRs in HUVECs, miR-146a, miR-9, miR-204 and miR-367 showed the highest up-regulation in senescent cells. Their predicted target genes belong to nine common pathways, including Toll-like receptor signalling (TLR) that plays a pivotal

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling

Olivieri

Lazzarini

Recchioni

et al. 2012

AGE

176

154

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“…Although studies found that the expression levels of miRNAs in certain immune cells changed with the aging process (Hackl et al 2010;Li et al 2012;Park et al 2013), whether these differentially expressed miRNAs are involved in regulating the biological function of the immune cells in the aging body is not fully understood. The expression profiles of miRNAs in the peritoneal macrophages of young and aged mice in LPS-induced acute inflammatory response were, for the first time, performed in our previous study using the miRNA microarray analysis.…”

mentioning

confidence: 99%

Dysregulated expression of miR-101b and miR-26b lead to age-associated increase in LPS-induced COX-2 expression in murine macrophage

Liú

Wang

et al. 2015

AGE

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Aging is the natural process of decline in physiological structure and function of various molecules, cells, tissues, and organs. Growing evidence indicates that increased immune genetic diversity and dysfunction of immune system cause aging-related pathophysiological process with the growth of age. In the present study, we observed that LPS-induced higher activation of cyclooxygenase (COX)-2 promoter is associated with the upregulated binding activity of nuclear factor kappa B (NF-κB) in peritoneal macrophages of aged mice than young ones. Additionally, COX-2 is a direct target of miR-101b and miR-26b in the macrophages. Significant upregulation of miR-101b and miR26b effectively prevented LPS-induced excessive expression of COX-2 in the young mice. Because these negative regulatory factors were unresponsive to LPS stimulation, the levels of COX-2 were markedly higher in the macrophages of aged mice. Further study showed that NF-κB activation contributed to the increase in the expression of miR-101b and miR-26b in the LPSstimulated macrophages of young mice, but not aged ones. Moreover, histone deacetylase (HDAC) inhibitor trichostatin A (TSA) upregulated expression of miR101b and miR-26b in the aged mouse macrophages only, but not the young cells. This demonstrated that HDAC suppressed the expression of miR-101b and miR-26b in the LPS-treated macrophages of aged mice and contributed to the aging process. TSA-induced increased expression of miR-101b and miR-26b could further suppress COX-2 expression. These findings provide novel evidence on the regulation of immune senescence and miR-101b and miR-26b, which might be promising targets in treating aged-related inflammatory diseases. Epigenetic regulation of the microRNAs (miRNAs) provides an important evidence for the treatment of innate inflammatory disease with HDAC inhibitors in elderly.

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“…[6][7][8][9] Furthermore, members of miR-17-92 cluster are found to be commonly down-regulated in aging human cells. 10 We have found that ectopic expression of miR-17 retards tissue growth 11 and inhibits cell senescence. 12 Piwi-interacting RNA (piRNA) is the largest class of small non-coding RNAs expressed by animal cells.…”

mentioning

confidence: 97%

Reciprocal regulation of miRNAs and piRNAs in embryonic development

Yang

Xuan

et al. 2016

Cell Death Differ

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MicroRNAs (miRNAs) and piwi-interacting RNAs (piRNAs) are two classes of small noncoding RNAs, both of which play roles in regulating tissue development. It is unknown whether these distinct classes of noncoding RNAs can regulate one another. Here we show that ectopic expression of miR-17 inhibited mouse fertility and early embryonic development. Specifically, we found that the piRNA amplification loop was repressed by miR-17-5p, leading to increased levels of transposition mutagenesis. This occurred by suppressing the amplification loop of piRNAs with an identical 5′ sequence and by targeting Mili/Miwi2, an essential component of the piRNA amplification loop, and the DNA methyltransferase, Dnmt3a. We also found that increased levels of piRNAs could compete with miRNAs for target binding, resulting in increased expression of Dnmt3a and Mili. Increased Dnmt3a levels could in turn block miR-17-5p expression, while increased Mili expression could accelerate piRNA amplification and inhibit transposon generation, favoring embryonic development. We report for the first time the reciprocal regulation between miRNAs and piRNAs in mouse embryonic development. Cell Death and Differentiation (2016) 23, 1458-1470 doi:10.1038/cdd.2016; published online 18 March 2016A microRNA (miRNA) is a small non-coding RNA molecule of 18-24 nucleotides in length that are post-transcriptional regulators of gene expression. A miRNA has the capacity to affect the stability of hundreds of unique mRNAs 1 and may repress synthesis of hundreds of proteins by base-pairing with the targeting mRNAs. 2 The discovery of miRNAs in gene regulation has improved our understanding of posttranscriptional control of tissue development and aging. 3-5 A polycistronic miRNA cluster, miR-17~92, consisting of six mature miRNAs , and miR-92a-1), has been reported to play a fundamental role in development and remodeling. [6][7][8][9] Furthermore, members of miR-17-92 cluster are found to be commonly down-regulated in aging human cells. 10 We have found that ectopic expression of miR-17 retards tissue growth 11 and inhibits cell senescence. 12 Piwi-interacting RNA (piRNA) is the largest class of small non-coding RNAs expressed by animal cells. 13 piRNAs form complexes with piwi proteins, which function posttranscriptionally in silencing retrotransposons and other genetic elements in germ-line cells. 14 piRNA activity in gene regulation may lead to silencing of transposon expression, 15 as most piRNA sequences are antisense to transposon sequences. 16 The activity of piRNAs in transposon silencing appears to be the most important event during embryonic development. 17 To facilitate silencing transposons in the testes of mammals or in the germ cells of invertebrates, the piwi proteins play essential roles in interacting with piRNAs.These piwi proteins are members of Argonautes, proteins that are needed for gene silencing in miRNA action, including MIWI, MIWI2 and MILI. The sequences of piRNAs guide the piwi proteins to their transposon targets. 17 Decreased expressio...

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miR‐17, miR‐19b, miR‐20a, and miR‐106a are down‐regulated in human aging

Cited by 325 publications

References 55 publications

MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling

MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling

Dysregulated expression of miR-101b and miR-26b lead to age-associated increase in LPS-induced COX-2 expression in murine macrophage

Reciprocal regulation of miRNAs and piRNAs in embryonic development

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