RNA-seq analysis of subcutaneous white adipose tissues from pancreatic tumor-bearing mice and non-tumor controls
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE274804 | GEO | 2026/03/17
REPOSITORIES: GEO
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Project description:In acute cold stress in mammals, JMJD1A, an H3K9 demethylase, up-regulates thermogenic gene expressions through β-adrenergic signaling in brown adipose tissue (BAT). Aside BAT-driven thermogenesis, mammals also have another mechanism to cope with long-term cold stress by inducing the browning of subcutaneous white adipose tissue (scWAT). Here, we show that this occurs through a two-step process that requires both β-adrenergic dependent phosphorylation of S265 and demethylation of H3K9me2 by JMJD1A. The histone demethylation independent acute Ucp1 induction in BAT and demethylation dependent chronic Ucp1 expression in beige-scWAT provide complementary molecular mechanisms to ensure an ordered transition between acute and chronic adaptation to cold stress. JMJD1A mediates two major signaling pathways, namlely β-adrenergic receptor and PPARγ activation, via PRDM16-PPARγ-P-JMJD1A complex for beige adipogenesis.
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Project description:In acute cold stress in mammals, JMJD1A, an H3K9 demethylase, up-regulates thermogenic gene expressions through β-adrenergic signaling in brown adipose tissue (BAT). Aside BAT-driven thermogenesis, mammals also have another mechanism to cope with long-term cold stress by inducing the browning of subcutaneous white adipose tissue (scWAT). Here, we show that this occurs through a two-step process that requires both β-adrenergic dependent phosphorylation of S265 and demethylation of H3K9me2 by JMJD1A. The histone demethylation independent acute Ucp1 induction in BAT and demethylation dependent chronic Ucp1 expression in beige-scWAT provide complementary molecular mechanisms to ensure an ordered transition between acute and chronic adaptation to cold stress. JMJD1A mediates two major signaling pathways, namlely β-adrenergic receptor and PPARγ activation, via PRDM16-PPARγ-P-JMJD1A complex for beige adipogenesis.
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Project description:We performed transcriptomic profiling for two models of adipose browning, the classical mouse model and our newly described great roundleaf bat (H. armiger) model. Transcriptomes were generated from subcutaneous adipose tissue (sWAT), intra-abdominal adipose tissue (aWAT) and interscapular BAT (iBAT) from male and female bats, as well as sWAT and iBAT from male and female mice, which were acclimatized to 10°C and 30°C. These 20 trascriptomes allowed us to identity genes, GO terms, and pathways that show significant expression changes and are shared by both species during the browning process.
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Project description:Timed-feeding leads to adipose browning, although the integrative mechanisms for the same remain unclear. Here we show that twice-a-nocturnal (TAN) feeding causes biphasic oscillations of circulating insulin and leptin, representing their entrainment by timed-feeding. Insulin and leptin surges lead to marked cellular, functional and metabolic remodeling of sWAT resulting in increased energy expenditure. Single-cell RNAseq analyses and flow cytometry reveal a role for insulin and leptin surges in ILC2 recruitment and sWAT browning, since depleting leptin or blocking insulin receptor signaling or ILC2 cell recruitment, each dampens TAN feeding-induced sWAT remodeling and energy expenditure. Consistently, recreating insulin and leptin oscillations via once-a-day co-injections is sufficient to favorably remodel innervated sWAT. Indeed, innervation is necessary for sWAT remodeling since denervation of sWAT, but not BAT, blocks TAN-induced sWAT remodeling and resolution of inflammation. In sum, timed feeding reorganizes nutrient-sensitive pathways to remodel sWAT, which drives the metabolic benefits of timed-feeding.
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