The mitochondrial lncRNA ASncmtRNA-2 is induced in aging and replicative senescence in Endothelial Cells

Bianchessi, Valentina; Badi, Ileana; Bertolotti, Matteo; Nigro, Patrizia; D’Alessandra, Yuri; Capogrossi, Maurizio C.; Zanobini, Marco; Pompilio, Giulio; Raucci, Angela; Lauri, Antonella

doi:10.1016/j.yjmcc.2015.01.012

Cited by 125 publications

(98 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several lncRNAs have recently been suggested to be involved in regulation of senescence, such as PANDA (13) and the mitochondrial lncRNA ASncmtRNA -2 (63). A recent study demonstrated upregulation of HOTAIR upon radiation-induced senescence in human fibroblasts (26).…”

Section: Discussionmentioning

confidence: 99%

The lncRNA HOTAIR impacts on mesenchymal stem cellsviatriple helix formation

et al. 2016

View full text Add to dashboard Cite

There is a growing perception that long non-coding RNAs (lncRNAs) modulate cellular function. In this study, we analyzed the role of the lncRNA HOTAIR in mesenchymal stem cells (MSCs) with particular focus on senescence-associated changes in gene expression and DNA-methylation (DNAm). HOTAIR binding sites were enriched at genomic regions that become hypermethylated with increasing cell culture passage. Overexpression and knockdown of HOTAIR inhibited or stimulated adipogenic differentiation of MSCs, respectively. Modification of HOTAIR expression evoked only very moderate effects on gene expression, particularly of polycomb group target genes. Furthermore, overexpression and knockdown of HOTAIR resulted in DNAm changes at HOTAIR binding sites. Five potential triple helix forming domains were predicted within the HOTAIR sequence based on reverse Hoogsteen hydrogen bonds. Notably, the predicted triple helix target sites for these HOTAIR domains were also enriched in differentially expressed genes and close to DNAm changes upon modulation of HOTAIR. Electrophoretic mobility shift assays provided further evidence that HOTAIR domains form RNA–DNA–DNA triplexes with predicted target sites. Our results demonstrate that HOTAIR impacts on differentiation of MSCs and that it is associated with senescence-associated DNAm. Targeting of epigenetic modifiers to relevant loci in the genome may involve triple helix formation with HOTAIR.

show abstract

Section: Discussionmentioning

confidence: 99%

The lncRNA HOTAIR impacts on mesenchymal stem cellsviatriple helix formation

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Moreover, the overexpression of the two miRNAs shows the similar phenotype, cell cycle delay in both the G1 and G2/M phases. They proposed that ASncmtRNA-2 is involved in replicative senescence in endothelial cells by causing cell cycle arrest in the transition from G2/M to G1 (112). …”

Section: Mitochondrial Lncrna Involved In Senescencementioning

confidence: 99%

Role of lncRNAs in Cellular Aging

Degirmenci

Sun

2016

Front. Endocrinol.

View full text Add to dashboard Cite

Aging is a universal, intrinsic, and time-dependent biological decay that is linked to intricate cellular processes including cellular senescence, telomere shortening, stem cell exhaustion, mitochondrial dysfunction, and deregulated metabolism. Cellular senescence is accepted as one of the core processes of aging at the organism level. Understanding the molecular mechanism underlying senescence could facilitate the development of potential therapeutics for aging and age-related diseases. Recently, the discovery of long non-coding RNAs (lncRNA) provided insights into a novel regulatory layer that can intervene with cellular senescence. Increasing evidence indicates that targeting lncRNAs may impact on senescence pathways. In this review, we will focus on lncRNAs involved in mechanistic pathways governing cellular senescence.

show abstract

“…Cell senescence can be divided into two categories, namely selfrepeating senescence and stress-induced premature senescence. The former is mainly caused by telomere shortening or dysfunction, while the latter is mainly induced by H 2 O 2 and ultraviolet, which arrest the cell cycle during the G1 phase (Sikora et al, 2011;Bianchessi et al, 2015). Mechanisms in both categories are involved in congenerous molecular signaling transduction pathways, such as the p16…”

Section: Introductionmentioning

confidence: 99%

Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

Li¹,

Yan²,

Zhang³

et al. 2016

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT. The development of age-related cardiovascular disease is associated with the senescence of vascular cells. This study aimed to investigate the effect of ginsenoside Rg1 on vascular smooth muscle cell (VSMC) senescence. Primary VSMCs were cultured and divided into control, D-galactose (D-gal), Rg1-L, and Rg1-H groups, which were cultured without and with D-gal, and with low-and highconcentrations of Rg1, respectively. D-gal-induced cellular senescence was identified by b-galactosidase staining, and ultrastructural changes within the cells were observed. The expression of p16, p21, and p53 in the four groups of VSMCs was determined by western blotting, and the cell cycle was investigated by flow cytometry. Compared with the control group, there was an obvious change in the ultrastructure of VSMCs in the D-gal group, and the proportion of b-galactosidasepositive cells was significantly increased (P < 0.05). In addition, p16, p21, and p53 expression was significantly increased (P < 0.05) and the cell cycle was arrested in the G0/G1 phase. Compared with the D-gal group, the percentage of positive cells was significantly reduced (P < 0.05) in the Rg1 groups, the expression of p16, p21, and p53 was significantly reduced (P < 0.05), and the number of cells in the G0/G1 phase decreased (P < 0.05). Ginsenoside Rg1 can inhibit VSMC senescence, and the mechanisms may be related to its partial inhibition of the p16 INK4a /Rb and p53-p21Cip1/Waf1 signaling pathways during the cell cycle.

show abstract

The mitochondrial lncRNA ASncmtRNA-2 is induced in aging and replicative senescence in Endothelial Cells

Cited by 125 publications

References 64 publications

The lncRNA HOTAIR impacts on mesenchymal stem cellsviatriple helix formation

The lncRNA HOTAIR impacts on mesenchymal stem cellsviatriple helix formation

Role of lncRNAs in Cellular Aging

Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

Contact Info

Product

Resources

About