Anti-senescent effects of long non-coding RNA H19 on human dermal fibroblast cells through impairing microRNA-296-5p-dependent inhibition of IGF2

Tang, Hua; Yao, Fang; Yin, Ming; Liao, Yangying; Li, Ke; Li, Lan; Xiao, Xiao; Guo, Junweichen; Hu, Feng; Feng, Hao

doi:10.1016/j.cellsig.2022.110327

Cited by 8 publications

(4 citation statements)

References 28 publications

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“…The epigenetic alterations largely reflect the aging-associated deleterious events. There is a loss of DNA methylation during aging and, with the advancement in age, genes such as estrogen receptor, insulin-like growth factor 2 (IGF2), and p16 are hypermethylated, with this abnormal DNA methylation leading to a heritable change [ 80 ]. Thus, the aged BBB could have its own profile of BBB recovery that reflects greater poststroke BBB leakage.…”

Section: Discussionmentioning

confidence: 99%

Epigenetics and stroke: role of DNA methylation and effect of aging on blood–brain barrier recovery

Phillips

Stamatovic

Keep

et al. 2023

Fluids Barriers CNS

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Incomplete recovery of blood–brain barrier (BBB) function contributes to stroke outcomes. How the BBB recovers after stroke remains largely unknown. Emerging evidence suggests that epigenetic factors play a significant role in regulating post-stroke BBB recovery. This study aimed to evaluate the epigenetic and transcriptional profile of cerebral microvessels after thromboembolic (TE) stroke to define potential causes of limited BBB recovery. RNA-sequencing and reduced representation bisulfite sequencing (RRBS) analyses were performed using microvessels isolated from young (6 months) and old (18 months) mice seven days poststroke compared to age-matched sham controls. DNA methylation profiling of poststroke brain microvessels revealed 11,287 differentially methylated regions (DMR) in old and 9818 DMR in young mice, corresponding to annotated genes. These DMR were enriched in genes encoding cell structural proteins (e.g., cell junction, and cell polarity, actin cytoskeleton, extracellular matrix), transporters and channels (e.g., potassium transmembrane transporter, organic anion and inorganic cation transporters, calcium ion transport), and proteins involved in endothelial cell processes (e.g., angiogenesis/vasculogenesis, cell signaling and transcription regulation). Integrated analysis of methylation and RNA sequencing identified changes in cell junctions (occludin), actin remodeling (ezrin) as well as signaling pathways like Rho GTPase (RhoA and Cdc42ep4). Aging as a hub of aberrant methylation affected BBB recovery processes by profound alterations (hypermethylation and repression) in structural protein expression (e.g., claudin-5) as well as activation of a set of genes involved in endothelial to mesenchymal transformation (e.g., Sox9, Snai1), repression of angiogenesis and epigenetic regulation. These findings revealed that DNA methylation plays an important role in regulating BBB repair after stroke, through regulating processes associated with BBB restoration and prevalently with processes enhancing BBB injury.

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Section: Discussionmentioning

confidence: 99%

Epigenetics and stroke: role of DNA methylation and effect of aging on blood–brain barrier recovery

Phillips

Stamatovic

Keep

et al. 2023

Fluids Barriers CNS

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“…Specifically, H19 lncRNA levels were decreased in aged human dermal fibroblasts. Their upregulation in these cells had a protective effect against senescence and enhanced cell viability [84]. On the other hand, the downregulation of the membrane-associated guanylate kinase WW and PDZ domain-containing 2 antisense RNA 3 (MAGI2-AS3) in human fibroblasts had a delaying effect on senescence [85].…”

Section: Lyplal1-as1 Suppresses Transcriptionmentioning

confidence: 99%

The Impact of Long Noncoding RNAs in Tissue Regeneration and Senescence

Tavares e Silva,

Pessoa,

Nóbrega-Pereira

et al. 2024

Cells

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Overcoming senescence with tissue engineering has a promising impact on multiple diseases. Here, we provide an overview of recent studies in which cellular senescence was inhibited through the up/downregulation of specific lncRNAs. This approach prevented senescence in the bones, joints, nervous system, heart, and blood vessels, with a potential impact on regeneration and the prevention of osteoarthritis and osteoporosis, as well as neurodegenerative and cardiovascular diseases. Senescence of the skin and liver could also be prevented through the regulation of cellular levels of specific lncRNAs, resulting in the rejuvenation of cells from these organs and their potential protection from disease. From these exciting achievements, which support tissue regeneration and are not restricted to stem cells, we propose lncRNA regulation through RNA or gene therapies as a prospective preventive and therapeutic approach against aging and multiple aging-related diseases.

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“…1.1.4 LncRNA H19-miR-296-5p-IGF2 axis in senescence of human dermal fibroblasts Tang et al (2022) investigated into the role of lncRNA H19 in human dermal fibroblasts (HDFs) concerning cellular viability and senescence. Their research led to the identification of miR-296-5p as a significant player in the regulation of these processes through a comparative analysis of young and aging skin samples.…”

Section: Introductionmentioning

confidence: 99%

LncRNA-miRNA-mRNA regulatory networks in skin aging and therapeutic potentials

Kim

2023

Front. Physiol.

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Skin aging is a complex process influenced by intrinsic and extrinsic factors. Although dermatology offers advanced interventions, molecular mechanisms in skin aging remain limited. Competing endogenous RNAs (ceRNAs), a subset of coding or non-coding RNAs, regulate gene expression through miRNA competition. Several ceRNA networks investigated up to now offer insights into skin aging and wound healing. In skin aging, RP11-670E13.6-miR-663a-CDK4/CD6 delays senescence induced by UVB radiation. Meg3-miR-93-5p-epiregulin contributes to UVB-induced inflammatory skin damage. Predicted ceRNA networks reveal UVA-induced photoaging mechanisms. SPRR2C sequesters miRNAs in epidermal aging-associated alteration of calcium gradient. H19-miR-296-5p-IGF2 regulates dermal fibroblast senescence. PVT1-miR-551b-3p-AQP3 influences skin photoaging. And bioinformatics analyses identify critical genes and compounds for skin aging interventions. In skin wound healing, MALAT1-miR-124 aids wound healing by activating the Wnt/β-catenin pathway. Hair follicle MSC-derived H19 promotes wound healing by inhibiting pyroptosis. And the SAN-miR-143-3p-ADD3 network rejuvenates adipose-derived mesenchymal stem cells in wound healing. Thus, ceRNA networks provide valuable insights into the molecular underpinnings of skin aging and wound healing, offering potential therapeutic strategies for further investigation. This comprehensive review serves as a foundational platform for future research endeavors in these crucial areas of dermatology.

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Anti-senescent effects of long non-coding RNA H19 on human dermal fibroblast cells through impairing microRNA-296-5p-dependent inhibition of IGF2

Cited by 8 publications

References 28 publications

Epigenetics and stroke: role of DNA methylation and effect of aging on blood–brain barrier recovery

Epigenetics and stroke: role of DNA methylation and effect of aging on blood–brain barrier recovery

The Impact of Long Noncoding RNAs in Tissue Regeneration and Senescence

LncRNA-miRNA-mRNA regulatory networks in skin aging and therapeutic potentials

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