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Impact of a pro-inflammatory stimulus on the miRNA composition of extracellular vesicles (EV) from stem cells from apical papilla (SCAP)

ABSTRACT: Impact of a pro-inflammatory stimulus on the miRNA composition of extracellular vesicles (EV) from stem cells from apical papilla (SCAP)

PROVIDER: PRJNA860164 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20313687.fastq.gz	Fastqsanger.gz
	SRR20313688.fastq.gz	Fastqsanger.gz
	SRR20313689.fastq.gz	Fastqsanger.gz
	SRR20313690.fastq.gz	Fastqsanger.gz
	SRR20313691.fastq.gz	Fastqsanger.gz

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Impact of a pro-inflammatory stimulus on the miRNA composition of extracellular vesicles (EV) from stem cells from apical papilla (SCAP)

Project description:To investigate the impact of a pro-inflammatory stimulus (TNFα and IFNγ, 20 ng/ml) on miRNA in SCAP-EV, we isolated EV from non-activated and activated SCAP and then extracted miRNA

2022-07-20 | GSE208577 | GEO

Transcriptional Profliing of small molecules induced endothelial cells of stem cells from apical papilla (SCAP-ECs), stem cells from apical papilla (SCAP) and human vein endothelial cells (HUVECs)

Project description:Recently, a new strategy has been developed to directly reprogram one cell type towards targeted cell type by using different combinations of small molecule compounds. Here we attempted to induce stem cells from apical papilla (SCAP) into endothelial cells (ECs) by the same strategy. We developed a set of small molecules and growth factors that facilitates the conversion of SCAP into stable endothelial lineage. The SCAP-derived endothelial cells (SCAP-ECs) expressed some up-regulated endothelial specific genes and proteins, exhibited the ability to form functional tubular-like structures in vitro, and contributed to generate blood vessels in vivo. The aim of this study is to compare the ECs-related gene profile of SCAP, SCAP-derived ECs and HUVECs (primary ECs) and to explore whether SCAP-derived ECs showed enriched ECs gene expression.

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Expression data of microRNA from human stem cells from apical papilla

Project description:Osteo/odontogenic differentiation is a key process of human stem cells from apical papilla (SCAP) in tooth root development. Emerging evidence indicates microRNAs (miRNAs) play diverse roles in osteogenesis. However, their functions in osteo/odontogenic differentiation of SCAP remain to be elucidated. We used miRNA microarray to analysis differentially expressed miRNAs in order to investigate the role of miRNAs in SCAP osteo/odontogenic differentiation and underlying mechanism.

2021-01-01 | GSE154466 | GEO

Transcriptional Profliing of small molecules induced endothelial cells of stem cells from apical papilla (SCAP-ECs), stem cells from apical papilla (SCAP) and human vein endothelial cells (HUVECs)

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The human dental apical papilla promotes spinal cord repair through a paracrine mechanism

Project description:Traumatic spinal cord injury is an overwhelming condition that strongly and suddenly impacts the patient’s life and her/his entourage. There are currently no predictable treatments to repair the spinal cord, while many strategies are proposed and evaluated by researchers throughout the world. One of the most promising avenues is the transplantation of stem cells, although its therapeutic efficiency is limited by several factors, among which cell survival at the lesion site. In our previous study, we showed that the implantation of a human dental apical papilla, residence of stem cells of the apical papilla (SCAP), supported functional recovery in a rat model of spinal cord hemisection.

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Comparative bulk RNAseq analysis of Control and Ctnnb1-deficient CXCL12+ apical papilla cells.

Project description:Lack of Ctnnb1 in CXCL12+ apical papilla cells causes a cell fate shift and fail to differentiate into root forming cells such as odontoblasts or cementoblasts. Here, we set out to reveal the transcriptome change induced by Ctnnb1 deficiency in CXCL12+ apical papilla cells

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Simvastatin modulates osteogenic differentiation in stem cells isolated from apical papilla

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Comparative bulk RNAseq analysis of Control and Ctnnb1-deficient CXCL12+ apical papilla cells.

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