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Single cell sequencing of stromal vascular fraction from facial infiltrating lipomatosis and normal facial adipose tissue

ABSTRACT: Single cell sequencing of stromal vascular fraction from facial infiltrating lipomatosis and normal facial adipose tissue

PROVIDER: PRJNA1112852 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29070762_1.fastq.gz	Fastqsanger.gz
	SRR29070762_2.fastq.gz	Fastqsanger.gz
	SRR29070763_1.fastq.gz	Fastqsanger.gz
	SRR29070763_2.fastq.gz	Fastqsanger.gz
	SRR29070764_1.fastq.gz	Fastqsanger.gz

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Single cell sequencing of stromal vascular fraction from facial infiltrating lipomatosis and normal facial adipose tissue

Project description:Facial infiltrating lipomatosis is characterized by excessive growth of adipose tissue, The etiology is associated with somatic PIK3CA variant, but the specific mechanisms are not yet fully understood. In this study, we collected facial adipose tissue from both FIL patients and non-FIL individuals, isolated the stromal vascular fraction (SVF) and performed single-cell transcriptome sequencing on these samples. We mapped out the cellular landscape within the SVF and specifically focused on a deeper analysis of fibro-adipogenic precursor cells (FAPs).

2024-07-06 | GSE267777 | GEO

Transcriptome sequencing of adipose tissue isolated from facial infiltrating lipomatosis or control

Project description:Facial infiltrating lipomatosis is a congenital malformation characterized primarily by the excessive proliferation of adipose tissue. However, the pathogenesis of it remains unclear. To compare the gene expression differences between the adipose tissue of facial infiltrating lipomatosis and normal facial subcutaneous adipose tissue, we collected a total of 14 adipose tissue samples for high-throughput RNA sequencing, aiming to identify potential pathogenic genes.

2026-02-20 | GSE300520 | GEO

Transcriptome sequencing of adipose tissue isolated from facial infiltrating lipomatosis or control

Project description:Transcriptome sequencing of adipose tissue isolated from facial infiltrating lipomatosis or control

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Effect of FKBP5 inhibitor SAFit2 on fibro-adipose progenitor cells isolated from facial infiltrating lipomatosis

Project description:Facial infiltrating lipomatosis (FIL) is a congenital disorder characterized by unilateral facial enlargement. Although next-generation sequencing has revealed that the pathogenesis of FIL is associated with phosphatidylinositol 3-kinase catalytic subunit alpha (PIK3CA) mutations, the underlying molecular mechanisms remain undetermined. We found that the adipose tissue in FIL patients demonstrated tissue infiltration accompanied by adipocytes hypertrophy and increased lipid accumulation. All FIL derived fibro-adipose progenitor cells (FIL-FAPs) harboured PIK3CA mutations. Compared to FAPs obtained from normal subcutaneous adipose tissue, FIL-FAPs exhibited a greater capacity for adipogenesis. Suppression of PIK3CA resulted in a reduction in the adipogenic potential of FIL-FAPs. Through single cell sequencing, we find that FIL-FAPs had higher expression of FKBP5. Inhibiting FKBP5 can impair the adipogenic capacity of FIL-FAPs. We also verified that PI3K-AKT pathway regulating FKBP5 expression. To find the downstream target of FKBP5, we performed RNA-seq of FIL-FAPs treated with FKBP5 inhibitor SAFit2 in DMSO or DMSO alone.

2025-08-08 | GSE279487 | GEO

Gene expression in canine adipose stromal vascular fraction

Project description:Microarray studies were performed to identify expression patterns by cryopreserved adipose stromal vascular fraction (SVF) preparations that were prepared by three different veterinary stem cell companies from the same source of canine adipose tissue.

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Comparison between stromal vascular fraction of adipose tissue, testis and epididymis in mouse

Project description:An experiment was performed in order to compare directly profiles of stromal vascular fraction of adipose tissue, testis and epidydimis, in order to rule out a possible contamination of the stromal vascular fraction of adipose tissue (SVF) by adjacent tissues (i.e. epididymis and testis). This led to the identification of a list of 2358 SVF-specific probes, which was subsequently used for further investigations. 3 dye-swap pairs, comparing 3 distinct samples of total RNA prepared from: (1) stromal vascular fraction of adipose tissue, (2) testis and (3) epidydimis.

2010-05-31 | E-GEOD-16613 | biostudies-arrayexpress

Effect of FKBP5 inhibitor SAFit2 on fibro-adipose progenitor cells isolated from facial infiltrating lipomatosis

Project description:Effect of FKBP5 inhibitor SAFit2 on fibro-adipose progenitor cells isolated from facial infiltrating lipomatosis

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Project description:immortalized ADSCs of Facial Infiltrating Lipomatosis

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Comparison between stromal vascular fraction of adipose tissue, testis and epididymis in mouse

2010-06-01 | GSE16613 | GEO

Effect of PI3K/mTOR dual-target inhibitor WX390 on adipose-derived stem cells isolated from facial infiltrating lipomatosis

Project description:Facial infiltrating lipomatosis (FIL) is a congenital disorder characterized by unilateral facial enlargement. Although next-generation sequencing has revealed that the pathogenesis of FIL is associated with phosphatidylinositol 3-kinase catalytic subunit alpha (PIK3CA) mutations, the underlying molecular mechanisms remain undetermined. We found that the adipose tissue in FIL patients demonstrated tissue infiltration accompanied by adipocytes hypertrophy and increased lipid accumulation. All FIL-ADSCs harboured PIK3CA mutations. Compared to ADSCs obtained from normal subcutaneous adipose tissue, FIL-ADSCs exhibited a greater capacity for adipogenesis. Suppression of PIK3CA resulted in a reduction in the adipogenic potential of FIL-ADSCs. Furthermore, WX390, a novel dual-target PI3K/mTOR inhibitor, was found to impede PIK3CA-mediated adipogenesis both in vivo and in vitro. RNA-seq revealed that the expression of transient receptor potential vanilloid subtype 1 (TRPV1) was upregulated after PI3K pathway inhibition, and overexpression and activation of TRPV1 both inhibited adipogenesis of FIL-ADSCs. Our study showed that PIK3CA mutations promoted adipogenesis in FIL-ADSCs and that this effect was achieved by suppressing the expression of TPRV1. Pathogenesis experiments suggested that WX390 may serve as an agent for the treatment of FIL.

2024-06-28 | GSE253170 | GEO

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