Effects of Pparγ1 deletion on late-stage murine embryogenesis and cells that undergo endocycle

Nakano, Takamitsu; Aochi, Hidekazu; Hirasaki, Masataka; Takenaka, Yasuhiro; Fujita, Koji; Tamura, Masahito; Soma, Hiroaki; Kamezawa, Hajime; Koizumi, Takahiro; Shibuya, Hirotoshi; Inomata, Reiko; Okuda, Akihiko; Murakoshi, Takayuki; Shimada, Akira; Inoue, Ituro

doi:10.1016/j.ydbio.2021.07.003

Cited by 3 publications

(2 citation statements)

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“…Notably, Pparγ1sv is significantly upregulated during adipocyte differentiation in these cells, and its knockdown via specific siRNAs substantially inhibits adipogenesis in 3T3-L1 cells. Pparγ1sv is ubiquitously expressed, with high levels in many tissues including the placenta and embryo [ 6 , 7 ]. Pparγ1sv -knockout (KO) mice are viable and fertile but exhibit a prolonged lower body weight during and after the weaning period [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

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Shared Mechanisms in Pparγ1sv and Pparγ2 Expression in 3T3‐L1 Cells: Studies on Epigenetic and Positive Feedback Regulation of Pparγ during Adipogenesis

Takenaka,

Kakinuma,

Ikeda

et al. 2024

PPAR Research

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We have previously reported the identification of a novel splicing variant of the mouse peroxisome proliferator‐activated receptor‐γ (Pparγ), referred to as Pparγ1sv. This variant, encoding the PPARγ1 protein, is abundantly and ubiquitously expressed, playing a crucial role in adipogenesis. Pparγ1sv possesses a unique promoter and 5 ′ untranslated region (5 ′UTR), distinct from those of the canonical mouse Pparγ1 and Pparγ2 mRNAs. We observed a significant increase in DNA methylation at two CpG sites within the proximal promoter region (‐733 to ‐76) of Pparγ1sv during adipocyte differentiation. Concurrently, chromatin immunoprecipitation‐quantitative PCR (ChIP‐qPCR) using antibodies against H3K4me3 and H3K27ac indicated marked elevations in both methylation and acetylation of histone H3, while the repressive histone mark H3K9me2 significantly decreased, at the transcription start sites of both Pparγ1sv and Pparγ2 following differentiation. Knocking down Pparγ1sv using specific siRNA also led to a decrease in Pparγ2 mRNA and PPARγ2 protein levels; conversely, knocking down Pparγ2 resulted in reduced Pparγ1sv mRNA and PPARγ1 protein levels, suggesting synergistic transcriptional regulation of Pparγ1sv and Pparγ2 during adipogenesis. Furthermore, our experiments utilizing the CRISPR‐Cas9 system identified crucial PPARγ‐binding sites within the Pparγ gene locus, underscoring their significance in adipogenesis. Based on these findings, we propose a model of positive feedback regulation for Pparγ1sv and Pparγ2 expression during the adipocyte differentiation process in 3T3‐L1 cells.

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Section: Introductionmentioning

confidence: 99%

“…Pparγ1sv is ubiquitously expressed, with high levels in many tissues including the placenta and embryo [ 6 , 7 ]. Pparγ1sv -knockout (KO) mice are viable and fertile but exhibit a prolonged lower body weight during and after the weaning period [ 7 ].…”

Section: Introductionmentioning

confidence: 99%