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The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence [chondrocytes part2]

ABSTRACT: Using large-scale patient data sets and genetically engineered (inducible conditional knockout and knockin) mouse models, we show that a novel transcript of long noncoding RNA ELDR is essential for the development of chondrocyte senescence.

ORGANISM(S): Mus musculus

PROVIDER: GSE178091 | GEO | 2021/06/20

REPOSITORIES: GEO

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The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence [chondrocytes part1]

Project description:Using large-scale patient data sets and genetically engineered (inducible conditional knockout and knockin) mouse models, we show that a novel transcript of long noncoding RNA ELDR is essential for the development of chondrocyte senescence.

2021-06-20 | GSE178090 | GEO

The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence [lncRNA]

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The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence [chondrocytes part2]

Project description:The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence [chondrocytes part2]

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The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence [chondrocytes part1]

Project description:The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence [chondrocytes part1]

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The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence

Project description:The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence

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Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-20 | GSE178092 | GEO

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MYL3 protects chondrocytes from senescence by inhibiting clathrin-mediated endocytosis and activating of Notch signaling

Project description:As the unique cell type in articular cartilage, chondrocyte senescence is a crucial cellular event contributing to osteoarthritis development. Here we show that clathrin-mediated endocytosis and activation of Notch signaling promotes chondrocyte senescence and osteoarthritis development, which is negatively regulated by myosin light chain 3. Myosin light chain 3 (MYL3) protein levels decline sharply in senescent chondrocytes of cartilages from model mice and osteoarthritis (OA) patients. Conditional deletion of Myl3 in chondrocytes significantly promoted, whereas intra-articular injection of adeno-associated virus overexpressing MYL3 delayed, OA progression in male mice. MYL3 deficiency led to enhanced clathrin-mediated endocytosis by promoting the interaction between myosin VI and clathrin, further inducing the internalization of Notch and resulting in activation of Notch signaling in chondrocytes. Pharmacologic blockade of clathrin-mediated endocytosis-Notch signaling prevented MYL3 loss-induced chondrocyte senescence and alleviated OA progression in mice. Our results establish a previously unknown mechanism essential for cellular senescence and provide a potential therapeutic direction for OA.

2023-09-07 | PXD044684 | Pride

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