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Identification of candidate genes simultaneously shared by adipogenesis and osteoblastogenesis from human mesenchymal stem cells

ABSTRACT: Identification of candidate genes simultaneously shared by adipogenesis and osteoblastogenesis from human mesenchymal stem cells

PROVIDER: PRJNA731536 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14608019_1.fastq.gz	Fastqsanger.gz
	SRR14608019_2.fastq.gz	Fastqsanger.gz
	SRR14608020_1.fastq.gz	Fastqsanger.gz
	SRR14608020_2.fastq.gz	Fastqsanger.gz
	SRR14608021_1.fastq.gz	Fastqsanger.gz

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Identification of candidate genes simultaneously shared by adipogenesis and osteoblastogenesis from human mesenchymal stem cells

Project description:we aimed to screen candidate genes of adipocyte/osteoblastogenesis using human mesenchymal stem cells (hMSCs) at 3, 5, and 7 days through RNA-Seq technique. The 275 significantly differentially expressed genes (DEGs) were identified simultaneously shared by two anecdotes. Furthermore, we confirmed that ANKRD1 (ankyrin repeat domain 1) facilitated adipogenesis and weaked osteoblastogenesis via RNA interference (RNAi), and IGF1 (insulin like growth factor 1) simultaneously enhancted adipo-osteoblastogenesis. This study would provide the potential molecular switches for the study of the balance of adipo-osteoblastogenesis and therapy of metabolic bone disease osteoporosis.

2021-05-21 | GSE174794 | GEO

The contribution of lipid droplets formation-related genes during adipogenesis to osteoblastogenesis

Project description:We tried to find out the contribution of lipid droplets formation-related genes during adipogenesis to osteoblastogenesis through RNA-Seq technique. Among the seventy-nine documented genes, APOB (apolipoprotein B), CES1 (carboxylesterase 1), and CIDEC (cell death inducing DFFA like effector c) were differentially expressed during osteoblastogenesis. We further confirmed gene function of APOB during osteoblastogenesis using lentivirus vector system. This study would provide the vital clues and molecular targets for balance regulation of hMSCs differentiation and new treatment strategy in metabolic bone diseases.

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The contribution of lipid droplets formation-related genes during adipogenesis to osteoblastogenesis

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Keratinocyte Wnt5β promotes dermal adipogenesis by simultaneously regulating adipocyte precursor cell conversion and adipogenic signaling

Project description:Keratinocyte Wnt5β promotes dermal adipogenesis by simultaneously regulating adipocyte precursor cell conversion and adipogenic signaling

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Gene expression profiles of differentiating BMSCs from WT and Irx5 knockout mice during osteoblastogenesis (day 4 post differentiation)

Project description:Functional mutagenic screening has been used to identify key factors required for a wide range of developmental processes. However, such screens can only be successfully applied in lower organisms. Here, through combined application of androgenetic haploid embryonic stem cells (haESCs) and CRISPR-Cas9-based genome editing, we quickly identify pivotal factors involved in early bone development from a medium-scale gene library. Injection of haESCs carrying constitutively expressed Cas9 and an sgRNA library containing 216 sgRNAs targeting 72 preselected candidate genes into oocytes produced biallelic mutant mice with high efficiency. Through skeletal phenotype analysis by Alcian blue and Alizarin Red staining at birth, we identified transcriptional factor Irx5 as a positive regulator of bone development. Irx5 KO mice generated by regular method exhibited obvious decreased bone mass and increased adipogenesis in the bone marrow. Moreover, the deletion of Irx5 from bone marrow cells prohibited osteoblast differentiation and enhanced adipocyte differentiation ability in vitro. Mechanistically, IRX5 promotes osteoblastogenesis and inhibits adipogenesis by suppressing PPARγ expression. We conclude that haESC-mediated SC technology, in combination with a targeted sgRNA library, can be used as a powerful reverse genetic screening strategy to identify pivotal factors involved in mouse development.

2019-12-30 | GSE117643 | GEO

Triazole fungicides induce adipogenesis and repress osteoblastogenesis in zebrafish.

Project description:Triazoles are a major group of azole fungicides commonly used in agriculture, and veterinary and human medicine. Maternal exposure to certain triazole antifungal medication causes congenital malformations, including skeletal malformations. We hypothesized that triazoles used as pesticides in agriculture also pose a risk of causing skeletal malformations in developing embryos. In this study, teratogenic effects of three commonly used triazoles, cyproconazole, paclobutrazol, and triadimenol, were investigated in zebrafish, Danio rerio. Exposure to the triazole fungicides caused bone and cartilage malformations in developing zebrafish larvae. Data from whole-embryo transcriptomics with cyproconazole suggested that exposure to this compound induces adipogenesis while repressing skeletal development. Confirming this finding, the expression of selected bone and cartilage marker genes were significantly downregulated with triazoles exposure as determined by quantitative PCR. The expression of selected adipogenic genes was upregulated by the triazoles. Furthermore, exposure to each of the three triazoles induced adipogenesis and lipid droplet formation in vitro in 3T3-L1 pre-adipocyte cells. In vivo in zebrafish larvae, cyproconazole exposure caused lipid accumulation. These results suggest that exposure to triazoles promotes adipogenesis at the expense of skeletal development, and thus they expand the chemical group of bona fide bone to fat switchers.

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Project description:Skin is the largest organ in the body and comprises several types of cells. The intercellular plasticity of keratinocytes, fibroblasts, and skin adipocytes contributes to wound healing and dermal adipogenesis. Although keratinocyte activates dermal adipose tissue (dWAT) differentiation upon hair follicular cycle, regulating dWAT hyperplasia through keratinocyte reprogramming is still unknown. We used the CRISPR/Cas9 base editor to induce single nucleotide polymorphisms in Forkhead-box N1 (Foxn1) and identified the p.L19M variant that induced the formation of a thicker dWAT regardless of hair follicular cycle or wound healing. Foxn1 p.L19M activates Wnt5β through transcriptional activity. Wnt5β signaling induces the conversion of dWAT dermal fibroblasts into adipose precursor cells (APCs) and promotes APC adipocyte differentiation through keratinocyte epithelial-mesenchymal transition (EMT) and adipogenic signaling. Wnt5β is involved in the entire process of dWAT hyperplasia through APC supply and adipogenic signaling as a single factor. Foxn1 p.L19M and Wnt5β are expressed in keratinocytes, and a keratinocyte-derived adipogenic signal is critical for dermal adipogenesis. In addition, transient expression of Foxn1 p.L19M or Wnt5β using adeno-associated virus reproduced dermal adipocyte hyperplasia in mice. Considering the increasing importance of dWAT in functions such as the immune response, wound healing, hair follicle growth, and temperature control, this finding has potential applications in skin regeneration

2023-08-05 | GSE239791 | GEO

Inhibiting DNA methylation switches adipogenesis to osteoblastogenesis by activating Wnt10a.

Project description:Both adipocytes and osteoblasts share the mesodermal lineage that derives from mesenchymal stem cells. Most studies investigating the mechanisms underlying the regulation of adipogenic or osteoblastogenic development focus on transcriptional pathways; little is known about the epigenetic mechanisms in this process. We thus determined the role of 5-aza-2'-deoxycytidine (5-Aza-dC), an inhibitor of DNA methylation, in the lineage determination between adipogenesis and osteoblastogenesis. Inhibiting DNA methylation in 3T3-L1 preadipocytes by 5-Aza-dC significantly inhibited adipogenesis whereas promoted osteoblastogenesis. This dual effect of 5-Aza-dC was associated with up-regulation of Wnt10a, a key factor determining the fate of the mesenchymal lineage towards osteoblasts. Consistently, IWP-2, an inhibitor of Wnt proteins, was found to prevent the anti-adipogenic effect of 5-Aza-dC in 3T3-L1 preadipocytes and block the osteoblastogenic effect of 5-Aza-dC in ST2 mesenchymal stem cell line. Finally, the Wnt10a 5'-region is enriched with CpG sites, whose methylation levels were markedly reduced by 5-Aza-dC. Thus we conclude that inhibiting DNA methylation by 5-Aza-dC mutual-exclusively regulates the lineage determination of adipogenesis and osteoblastogenesis by demethylating Wnt10a gene and upregulating its expression. Our study defines DNA methylation as a novel mechanism underlying adipocyte and bone cell development.

| S-EPMC4853709 | biostudies-literature

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DEPTOR cell-autonomously promotes adipogenesis and associates with obesity

Project description:An understanding of the mechanisms regulating white adipose tissue (WAT) formation is key for developing of new tools to treat obesity and its related diseases. Here, we identify DEPTOR as a positive regulator of adipogenesis whose expression is associated with obesity. In a polygenic mouse model of obesity/leanness, Deptor is part of the Fob3a QTL linked to obesity and we fine that Deptor is the highest priority candidate gene regulating WAT accumulation in this model. Using a doxycycline-inducible mouse model for Deptor overexpression, we confirmed that Deptor promotes WAT expansion in vivo. DEPTOR expression is elevated in WAT of obese humans and strongly correlates with the degree of obesity. We show that DEPTOR is induced during adipogenesis and that its overexpression cell-autonomously promotes, while its suppression blocks, adipogenesis. DEPTOR positively regulates adipogenesis by promoting the activity of the pro-adipogenic factors Akt/PKB and PPAR-gamma. These results establish DEPTOR as a physiological regulator of adipogenesis and provide new insights into the molecular mechanisms controlling WAT formation. 2 groups of F2 mice for opossing genotype at Fob3a QTL (FF versus VV) - parental strains of the F2 cross were the Fat line and congenic V-line; 5 biological replications per group; reference for Fat line: Horvat S. et al. (2000) MAMMALIAN GENOME 11(1): 2-7

2012-08-14 | E-GEOD-38321 | biostudies-arrayexpress

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