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KLF2 may suppress chicken adipogenesis by enhancing the GATA2 transcription

ABSTRACT: Kruppel-like factor 2 (KLF2) acts as an essential modulator of adipogenesis; nevertheless, the exact molecular pathways governing its role remain uncharacterized. This investigation characterized the expression profile of KLF2 in human adipose tissue and elucidated the mechanisms by which KLF2 modulates adipogenesis in avian models. The KLF2 mRNA expression in human adipose tissues was substantial and exhibited significant heterogeneity influenced by gender and anatomical location, suggesting that KLF2 regulated adipose tissue functionality. In chicken preadipocytes ICP1, the KLF2 protein increased at the first 24 h of oleate-induced adipogenic differentiation and subsequently decreased over time. KLF2 facilitated the cellular proliferation of ICP1 cells (P<0.05). Moreover, KLF2 overexpression inhibited differentiation of chicken preadipocytes ICP1 (P<0.05). KLF2 also increased the density of mitochondria and mitochondrial cristae in ICP1 cells. RNA seq and luciferase reporter assays demonstrated that KLF2 suppressed the expression of genes in PPAR signaling pathway in ICP1 cells. Additionally, KLF2 interacted with the promoter region of chicken GATA2 and upregulated GATA2 transcription in ICP1 cells. In summary, KLF2 potentially influences the PPAR signaling cascade, mitochondrial bioenergetics, and GATA2 gene expression to enhance the proliferation of avian preadipocytes while inhibiting their differentiation.

ORGANISM(S): Gallus gallus

PROVIDER: GSE302747 | GEO | 2025/07/17

REPOSITORIES: GEO

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Project description:Full title: Expression data from human primary subcutaneous preadipocytes treated with glucocorticoids prior to the initiation of differentiation. Preadipocytes are continuously exposed to glucocorticoids in situ due to both steroid present in the circulatory system as well as adipose tissue specific 11Î²HSD1 activity. While the effects of glucocorticoids during differentiation are well studied, the effect of exposure of preadipocytes to glucocorticoids prior to differentiation is unknown. We therefore treated confluent human primary preadipocytes drived from subcutaneous adipose tissue with the synthetic glucocorticoid dexamethasone for 48 hours prior to the initiation of differentiation and assessed what effect this had on their subsequent potential to differentiate. We found that pretreatment with glucocorticoids had a priming effect and resulted in increased differentiation of these preadipocytes. Furthermore, this treatment was additive to the effects of glucocorticoids during the initial phase of adipogenesis. Microarray analysis performed subsequent to the pretreatment with glucocorticoids (at the time point at which preadipocytes would have been induced to differentiate) identified glucocorticoid-responsive, candidate genes whose altered expression could mediate these effects. keywords: glucocorticoids, glucocorticoid receptor, preadipocytes, adipogenesis, human primary preadipocytes, subcutaneous, adipose tissue Experiment Overall Design: Human subcutaneous primary preadipocytes were purchased from Zen-Bio Inc. Preadipocytes from 5 female donors (average BMI 22.5Â±0.2kg/m2) were pooled prior to the initial seeding in T75 flasks. Cells were maintained at 5% CO2 in DMEM with 1.0g/L glucose, 20% calf serum, 100U/ml penicillin, 100mg/ml streptomycin and 50U/ml nystatin. Cells were expanded once prior to seeding in Nunc-brand 12-well dishes. Upon reaching confluence (24 h post-splitting), preadipocytes were stimulated with vehicle or 1uM dex for 48 hours in growth media containing 3% calf serum. Microarray analysis was performed on duplicate samples.

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KLF2 may suppress chicken adipogenesis by enhancing the GATA2 transcription

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