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NAP1L2 Drives Mesenchymal Stem Cell Senescence and Suppresses Osteogenic Differentiation

ABSTRACT: NAP1L2 Drives Mesenchymal Stem Cell Senescence and Suppresses Osteogenic Differentiation

PROVIDER: PRJNA699762 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13639811_1.fastq.gz	Fastqsanger.gz
	SRR13639811_2.fastq.gz	Fastqsanger.gz
	SRR13639812_1.fastq.gz	Fastqsanger.gz
	SRR13639812_2.fastq.gz	Fastqsanger.gz
	SRR13639813_1.fastq.gz	Fastqsanger.gz

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NAP1L2 Drives Mesenchymal Stem Cell Senescence and Suppresses Osteogenic Differentiation [ChIP-Seq]

Project description:NAP1L2 Drives Mesenchymal Stem Cell Senescence and Suppresses Osteogenic Differentiation [ChIP-Seq]

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NAP1L2 Drives Mesenchymal Stem Cell Senescence and Suppresses Osteogenic Differentiation [RNA-Seq]

Project description:NAP1L2 Drives Mesenchymal Stem Cell Senescence and Suppresses Osteogenic Differentiation [RNA-Seq]

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NAP1L2 Drives Mesenchymal Stem Cell Senescence and Suppresses Osteogenic Differentiation [RNA-Seq]

Project description:Changes in these genes are probably a consequence of aging, and the real regulators governing BMSC senescence and osteogenesis are still unclear.In the current study, we report that nucleosome assembly-related protein NAP1L2 serves as an important regulator of both the senescence and osteogenic differentiation of BMSCs through inhibition of NF-κB signaling and recruitment of SIRT1 to deacetylate the H3K14ac level on promoters of osteogenic genes. Thus, targeting NAP1L2 using an aging antagonist such as NMN would benefit aging-related disease.

2021-02-06 | GSE166243 | GEO

NAP1L2 Drives Mesenchymal Stem Cell Senescence and Suppresses Osteogenic Differentiation [ChIP-Seq]

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NAP1L2 drives mesenchymal stem cell senescence and suppresses osteogenic differentiation.

Project description:Senescence of bone marrow mesenchymal stem cells (BMSCs) impairs stemness and osteogenic differentiation, but the key regulators for senescence and the related osteogenesis are not well defined. Herein, we screened the gene expression profiles of human BMSCs from young and old donors and identified that elevation of the nucleosome assembly protein 1-like 2 (NAP1L2) expression was correlated with BMSC senescence and impaired osteogenesis. Elevated NAP1L2 expression was observed in replicative cell senescence and induced cell senescence in vitro, and in age-related senescent human and mouse BMSCs in vivo, concomitant with significantly augmented chromatin accessibility detected by ATAC-seq. Loss- and gain-of-functions of NAP1L2 affected activation of NF-κB pathway, status of histone 3 lysine 14 acetylation (H3K14ac), and chromatin accessibility on osteogenic genes in BMSCs. Mechanistic studies revealed that NAP1L2, a histone chaperone, recruited SIRT1 to deacetylate H3K14ac on promoters of osteogenic genes such as Runx2, Sp7, and Bglap and suppressed the osteogenic differentiation of BMSCs. Importantly, molecular docking analysis showed a possible bond between NAP1L2 and an anti-aging reagent, the nicotinamide mononucleotide (NMN), and indeed, administration of NMN alleviated senescent phenotypes of BMSCs. In vivo and clinical evidence from aging mice and patients with senile osteoporosis also confirmed that elevation of NAP1L2 expression was associated with suppressed osteoblastogenesis. Taken together, our findings suggest that NAP1L2 is a regulator of both BMSC cell senescence and osteogenic differentiation, and provide a new theoretical basis for aging-related disease.

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Project description:Epigenetic Plasticity Drives Adipogenic and Osteogenic Differentiation of Marrow-Derived Mesenchymal Stem Cells

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NAP1L2 Drives Mesenchymal Stem Cell Senescence and Suppresses Osteogenic Differentiation

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

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MicroRNA profiling of human umbilical cord mesenchymal stem cells during osteogenic differentiation

Project description:The time course experiment was designed as follow: (1) Mesenchymal stem cell (indifferentiated cells)/ time 0h; (2) After 24 h of osteogenic induction; (3) After 48 h of osteogenic induction (4) After 7 days of osteogenic induction.

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Project description:Comprehensive analyses of miRNAs expression were performed using miRNA microarrays during osteogenic differentiation of PDGFRa+ mesenchymal progenitors isolated from human skeletal muscle to identify miRNAs that are involved in osteogenesis of PDGFRa+ mesenchymal progenitors. PDGFRa+ mesenchymal progenitors were isolated from the gluteus medius muscles of two different patients, and then subjected to osteogenic induction. Expression of miRNAs was examined using miRNA microarrays at the time points of one week and two weeks after osteogenic induction and were compared with that of uninduced cells.

2013-08-01 | E-GEOD-39361 | biostudies-arrayexpress

Epigenetic Plasticity Drives Adipogenic and Osteogenic Differentiation of Marrow-Derived Mesenchymal Stem Cells (RNA-seq)

Project description:Terminal differentiation of multipotent stem cells is achieved through a coordinated cascade of activated transcription factors and epigenetic modifications that drive gene transcription responsible for unique cell fate. Within the mesenchymal lineage, factors such as RUNX2 and PPARγ are indispensable for osteogenesis and adipogenesis, respectively. We therefore investigated genomic binding of transcription factors and accompanying epigenetic modifications that occur during osteogenic and adipogenic differentiation of mouse bone marrow-derived mesenchymal stem cells (MSC). As assessed by ChIP-seq and RNA-seq analyses, we found that genes vital for osteogenic identity were linked to RUNX2, C/EBPβ, RXR, and VDR binding sites, whereas adipocyte differentiation favored PPARγ, RXR, C/EBPα, and C/EBPβ binding sites. Epigenetic marks were clear predictors of active differentiation loci as well as enhancer activities and selective gene expression. These marrow-derived MSCs displayed an epigenetic pattern that suggested a default preference for the osteogenic pathway; however, these patterns were rapidly altered near the Adipoq, Cidec, Fabp4, Lipe, Plin1, Pparg and Cebpa genes during adipogenic differentiation. Surprisingly, we found that these cells also exhibited an epigenetic plasticity that enabled them to trans-differentiate from adipocytes to osteoblasts (and vice-versa) after commitment, as assessed by staining, gene expression, and ChIP-qPCR analysis. The osteogenic default pathway may be subverted during pathological conditions leading to skeletal fragility and increased marrow adipocity during aging, estrogen deficiency and skeletal unloading. Taken together, our data provide an increased mechanistic understanding of the epigenetic programs necessary for multipotent differentiation of MSCs that may prove beneficial in the development of therapeutic strategies.

2016-07-11 | GSE79814 | GEO

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