ArticleCell & bioscience2022
LncRNA LYPLAL1-AS1 rejuvenates human adipose-derived mesenchymal stem cell senescence via transcriptional MIRLET7B inactivation.
Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Clinical application of mesenchymal stem cells in immunosenescence: a qualitative review of their potential and challenges.Stem cell research & therapy · 2025Review
- Mesenchymal Stem Cells Senescence: Mechanism and Rejuvenation Interventions.International journal of medical sciences · 2025Review
- Recent Advances in Hydrogel Technology in Delivering Mesenchymal Stem Cell for Osteoarthritis Therapy.Biomolecules · 2024Review
- The Rejuvenation and Functional Restoration of Aged Adipose Stem Cells by DUXAP10 Knockdown via the Regulation of the miR-214-3p/RASSF5 Axis.Stem cells translational medicine · 2024Article
- Review
- A novel molecular subtypes and risk model based on inflammatory response-related lncrnas for bladder cancer.Hereditas · 2022Article
- Natural antisense transcripts as drug targets.Frontiers in molecular biosciences · 2022Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMesenchymal stem cell (MSC) senescence is a phenotype of aging. Long noncoding RNAs (lncRNAs) are emerging as potential key regulators of senescence. However, the role of lncRNAs in MSC senescence remains largely unknown.
resultsWe performed transcriptome analysis in senescent human adipose-derived MSCs (hADSCs) and identified that the lncRNA LYPLAL1 antisense RNA1 (LYPLAL1-AS1) was significantly downregulated in senescent hADSCs. LYPLAL1-AS1 expression in peripheral blood was lower in middle-aged healthy donors than in young adult donors, and correlated negatively with age. Knockdown of LYPLAL1-AS1 accelerated hADSC senescence, while LYPLAL1-AS1 overexpression attenuated it. Chromatin isolation by RNA purification (ChIRP) sequencing indicated that LYPLAL1-AS1 bound to the MIRLET7B promoter region and suppressed its transcription activity, as demonstrated by dual-luciferase assay. miR-let-7b, the transcript of MIRLET7B, was upregulated during hADSC senescence and was regulated by LYPLAL1-AS1. Furthermore, miR-let-7b mimics promoted hADSC senescence, while the inhibitors repressed it. Finally, LYPLAL1-AS1 overexpression reversed miR-let-7b-induced hADSC senescence.
conclusionsOur data demonstrate that LYPLAL1-AS1 rejuvenates hADSCs through the transcriptional inhibition of MIRLET7B. Our work provides new insights into the mechanism of MSC senescence and indicates lncRNA LYPLAL1-AS1 and miR-let-7b as potential therapeutic targets in aging.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.