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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 circular RNAs 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 piRNAs in early osteogenic and chondrogenic differentiation of human bone marrow-mesenchymal stromal cells (hMSCs)

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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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Differentially Expressed piRNAs in TAC-induced mouse cardiac hypertrophy

Project description:To systematically investigate the potential role of piRNA(s) and for the identification of specific piRNA(s) dysregulated in cardiac hypertrophy, we examined the global expression profile of piRNAs in left ventricle samples obtained 4 weeks after TAC surgery in adult mice.

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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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Changes in gene expression of hMSCs and NOD/scid mouse lung after IV infusion of hMSCs

Project description:Quantitative assays for human DNA and mRNA were used to examine the paradox that intravenously (IV) infused human multipotent stromal cells (hMSCs) can enhance tissue repair without significant engraftment. After 2 X 106 hMSCs were IV infused into mice, most of the cells were trapped as emboli in lung. The cells in lung disappeared with a half-life of about 24 hr but < 1,000 cells appeared in 6 other tissues. The hMSCs in lung up-regulated expression of multiple genes with a large increase in the anti-inflammatory protein TSG-6. After myocardial infarction, IV hMSCs but not hMSCs transduced with TSG-6 siRNA decreased inflammatory responses, reduced infarct size, and improved cardiac function. IV administration of recombinant TSG-6 also reduced inflammatory responses and reduced infarct size. The results suggest improvements in animal models and patients after IV infusions of MSCs are at least in part explained by activation of MSCs to secrete TSG-6.

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