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Identification of differentially-expressed piRNAs after human bone marrow-mesenchymal stromal cells (hMSCs) detachment

ABSTRACT: Identification of differentially-expressed piRNAs after human bone marrow-mesenchymal stromal cells (hMSCs) detachment

PROVIDER: PRJNA530998 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8856240.fastq.gz	Fastqsanger.gz
	SRR8856241.fastq.gz	Fastqsanger.gz
	SRR8856242.fastq.gz	Fastqsanger.gz
	SRR8856243.fastq.gz	Fastqsanger.gz
	SRR8856234.fastq.gz	Fastqsanger.gz

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Identification of differentially-expressed miRNAs after human bone marrow-mesenchymal stromal cells (hMSCs) detachment

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Identification of differentially-expressed piRNAs after human bone marrow-mesenchymal stromal cells (hMSCs) detachment

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Identification of differentially-expressed miRNAs after human bone marrow-mesenchymal stromal cells (hMSCs) detachment

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Identification of differentially-expressed circular RNAs after human bone marrow-mesenchymal stromal cells (hMSCs) detachment

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Project description:The aim of this study was to identify non-coding RNA that were differentially expressed 7 days after induction of osteogenic or chondrogenic differentiation in human bone marrow-mesenchymal stromal cells (MSCs).

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Impacts of Inorganic Arsenic Exposure on Genetic Stability of Human Mesenchymal Stromal Cells (hMSCs)

Project description:Human mesenchymal stem/stromal cells (hMSCs) can differentiate into mesoderm-type cells, making them suitable candidates for tissue repair therapies. However, their relatively low frequency in adult tissue necessitates ex vivo expansion prior to regenerative medicine applications. Expansion can lead to selection of chromosomally abnormal clones and therefore, long-term hMSC stability should be studied. hMSCs applications in regenerative medicine ensures commercial availability of normal karyotype human primary cells for toxicity assessment and hMSCs could serve as alternatives to immortalized human cell models. In this work, we evaluated the potential of hMSCs in toxicity testing using inorganic arsenic (iAs) as a case study. hMSCs were exposed to iAs at different durations to track cellular aging and study long-term genetic stability. iAs exposures (48 hours) resulted in micronuclei induction. hMSCs were also exposed to iAs for 6 days to determine if hMSCs would become more susceptible to chromosomal damage following exposure to the model genotoxicant, mitomycin C (MMC). The culture duration and iAs exposure did not alter MMC potency, indicating that the hMSCs susceptibility to chromosomal damage remained unchanged. We also used gene expression analysis to investigate the molecular impacts of iAs on hMSCs over the course of short (3 days total) and long (30 days total) experiments. Both iAs exposures activated biomarkers associated with oxidative stress, but not biomarkers for direct DNA damage, providing support for an indirect mode of action for iAs genotoxicity. Overall, this study establishes the utility of hMSCs as a new model for toxicity screening and provides mechanistic information underlying iAs toxicity.

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Stabilizing heterochromatin by ZKSCAN3 safeguards hMSCs from senescence

Project description:Zinc finger protein with KRAB and SCAN domain 3 (ZKSCAN3), a transcriptional repressor, involves in multiple cellular functions. However, the functions of ZKSCAN3 in the homeostatic maintenance of human stem cells remains elusive. Here, we demonstrated that ZKSCAN3 was crucial for preventing human mesenchymal stem cells (hMSCs) from senescence in an autophagy-independent manner. Downregulation of ZKSCAN3 was observed in senescent hMSCs, and depletion of ZKSCAN3 led to premature aging in hMSCs. Further study uncovered that ZKSCAN3 maintained heterochromatin (HC) stability by interacting with heterochromatin associated proteins KAP1 and HP1 as well as nuclear envelope proteins Lamin B1, LBR and Emerin. Deficiency of ZKSCAN3 resulted in detachment of Lamina-associated domains (LADs) from the lamina, loss of heterochromatin and more accessible chromatin status within the heterochromatin and aberrant expression of repetitive sequences. Overexpression of ZKSCAN3, KAP1 or HP1 respectively rescued the senescent phenotypes in ZKSCAN3-/- hMSCs. Notably, reintroduction of ZKSCAN3 protein also retarded the cellular senescence in the replicative senescent hMSCs, as well as the pathological or physiological aging hMSCs. Together, our study reveals a novel, autophagy-independent role of ZKSCAN3 in the maintenance of heterochromatin stability and attenuation of hMSC senescence. Thus, ZKSCAN3 may be a candidate for alleviating human aging-related disorders.

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