| 27917303 | PURPOSE: MicroRNA-146a (miR-146a) has been proposed as a marker for age-associated inflammation, or "inflammaging", acting as a negative regulator of cellular senescence and pro-inflammatory signaling pathways |
| 27917303 | METHODS: The expression of miR-146a and miR-146b was examined in the neuroretina and RPE/choroid in mice aged from 2 months to 24 months |
| 27917303 | Then, the effect of synthetic miR-146a mimetic on IL-6 and VEGF-A expression was analyzed in RPE cells treated with and without TNF-alpha |
| 27917303 | RESULTS: miR-146a and miR-146b was upregulated during aging of RPE/choroid but not neuroretina, supporting tissue-specific regulation of aging-related miRNAs in retinal tissues |
| 27917303 | Overexpression of miR-146a by miRNA mimics inhibited VEGF-A and TNF-alpha-induced IL-6 expression |
| 27917303 | CONCLUSIONS: Elevation of miR-146a and miR-146b in the aging RPE/choroid but not neuroretina suggests a role for miRNAs in inflammaging in the RPE/choroid |
| 26390028 | MiRNAs profiling analysis in YMSCs and OMSCs by microarray showed that miR-140, miR-146a/b, and miR-195 were significantly upregulated in OMSCs, which led us to hypothesize that these are age-induced miRNAs involved in stem cell senescence |
| 25448133 | We focused on the hormonal aging and on the interaction between HRT use and the modulation of miR-21, miR-146a and classical inflammation markers |
| 25448133 | Serum miR-21 and miR-146a levels and FasL concentrations were lower in HRT users compared to their non-using co-twins, demonstrating their responsiveness to HRT |
| 25093579 | Other miRNAs, including miR-146a, show a more T-cell-subset-specific expression pattern and are involved in the regulation of processes unique to that specific T-cell subset |
| 24917789 | These findings together with the reduced expression of microRNA (miR)-124, and miR-155, decreased autophagy, enhanced senescence associated beta-galactosidase activity and elevated miR-146a expression, are suggestive that 16 DIV cells mainly correspond to irresponsive/senescent microglia |
| 24607549 | MitomiRs in human inflamm-aging: a hypothesis involving miR-181a, miR-34a and miR-146a |
| 24607549 | Here we show that some mitomiRs (let7b, mir-146a, -133b, -106a, -19b, -20a, -34a, -181a and -221) are also among the miRs primarily involved in cell aging and in inflamm-aging |
| 24607549 | This intriguing hypothesis is supported by several observations: i) in endothelial cells undergoing replicative senescence (HUVECs), a well-established model of cell senescence, miR-146a, miR-34a, and miR-181a are over-expressed whereas their target Bcl-2 is down-regulated; ii) IPA of the miR-146a, miR-34a and miR-181a network shows that they are closely linked to each other, to Bcl-2 and to mitochondria; and iii) miR-146a, miR-34a, and miR-181a are involved in important cell functions (growth, proliferation, death, survival, maintenance) and age-related diseases (cancer, skeletal and muscle disorders, neurological, cardiovascular and metabolic diseases) |
| 23832538 | Among the significantly UVA-downregulated miRNAs, miR-146a overexpression antagonized the UVA-induced proliferation inhibition and suppressed the upregulation of aging-related genes in photoaging of our model |
| 23832538 | Western blot and luciferase assay showed that Smad4 might be a target of miR-146a to exert miR-146a functions during photoaging |
| 23832538 | Therefore, UVA radiation-induced photoaging results in specific patterns of miRNA response and miR-146a are able to antagonize UVA-caused photoaging partially through targeting Smad4 |
| 23727324 | Anti-inflammatory effect of ubiquinol-10 on young and senescent endothelial cells via miR-146a modulation |
| 23727324 | We previously reported that a biomarker combination including miR-146a, its target protein IL-1 receptor-associated kinase (IRAK-1), and released interleukin (IL)-6, here collectively designated as MIRAKIL, indicates senescence-associated secretory phenotype (SASP) acquisition by primary human umbilical vein endothelial cells (HUVECs) |
| 23727324 | However, short-term CoQ10H(2) supplementation attenuated LPS-induced MIRAKIL changes in young cells; in senescent cells CoQ10H(2) supplementation significantly attenuated LPS-induced miR-146a and IRAK-1 modulation but failed to curb IL-6 release |
| 23252865 | We demonstrated that the expressions of myelogenic miRNAs such as miR-155, miR-223, miR-146a, miR-146b, miR-132, miR-142-5p, and miR-142-3p were increased in aged bone marrow derived dendritic cells (BMDC) under normal and activated conditions |
| 23252865 | We also observed that the expressions of IRAK1 and TRAF6, the targets of miR-146a, and DC-SIGN, a target of miR-155 were diminished while miR-146a and miR-155 were augmented during aging |
| 22692818 | MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling |
| 22692818 | Among the 367 profiled miRs in HUVECs, miR-146a, miR-9, miR-204 and miR-367 showed the highest up-regulation in senescent cells |
| 22692818 | MiR-146a was the most up-regulated miR in the validation analysis (>10-fold) |
| 22692818 | Significant correlations were observed among miR-146a expression and beta-galactosidase expression, telomere length and telomerase activity |
| 22692818 | MiR-146a hyper-expression was also validated in senescent HAECs (>4-fold) and HCAECs (>30-fold) |
| 22692818 | Therefore, we also included miR-146a expression determination in CACs from 37 CHF patients and 35 healthy control subjects (CTR) for this study |
| 22692818 | Interestingly, a 1,000-fold increased expression of miR-146a was observed in CACs of CHF patients compared to CTR, along with decreased expression of IRAK1 protein |
| 22692818 | Moreover, significant correlations among miR-146a expression, telomere length and telomerase activity were observed |
| 22692818 | Overall, our findings indicate that miR-146a is a marker of a senescence-associated pro-inflammatory status in vascular remodelling cells |
| 21511256 | METHODS AND RESULTS: Through a microarray approach, we have identified a miR-146a that is progressively modulated in endothelial cells with aging |
| 21511256 | CONCLUSIONS AND GENERAL SIGNIFICANCE: Finding important factors that regulate endothelial cell senescence, like miR-146a, will help provide novel therapeutic strategies for vascular disorders |
| 20824140 | Importantly, the comparison of late passage immortalized fibroblasts to senescent wild type fibroblasts reveals that miR-146a, a miRNA with a validated role in regulating the senescence associated secretory pathway, is also regulated during extended cell culture independently of senescence |
| 20053980 | Modulation of inflammatory markers by miR-146a during replicative senescence in trabecular meshwork cells |
| 20053980 | The effects of miR-146a on gene expression were analyzed with gene arrays and the results confirmed by real-time q-PCR |
| 20053980 | RESULTS: RS of HTM cells was associated with significant changes in expression of 18 miRNAs, including the upregulation of miR-146a |
| 20053980 | Upregulation of the anti-inflammatory miR-146a may serve to restrain excessive production of inflammatory mediators in senescent cells and limit their deleterious effects on the surrounding tissue |
| 20053980 | Among the different proteins repressed by miR-146a, the inhibition of PAI-1 may act to minimize the effects of senescence on the generation of iROS and growth arrest and prevent alterations of the extracellular proteolytic activity of the TM |
