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Effect of PDK4 or ACSS2 knockdown on HASMC phenotype after 7 days of treatment [RNAseq-siPDK4-siACSS2]

ABSTRACT: We find that PDK4 knockdown mimics the effect of TGFb in HASMCs, inducing SMC glycolysis and contractile gene expressions. Wherase, ACSS2 knockdown decreases glycolysis and contractile gene expressions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE288831 | GEO | 2025/09/01

REPOSITORIES: GEO

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TGFβ maintains smooth muscle cell contractile phenotype via PDK4-dpendent regulation of Ac-CoA production [ATAC-Seq_TGF-siPDK4]

Project description:We find that TGFβ signaling in SMCs induced ACSS2-dependent production of Ac-CoA in a PDK4-dependent manner. TGFb induces SMC contractile phenotype and glycolysis.

2025-09-01 | GSE288977 | GEO

Effect of TGFb on HASMC phenotype after 7 days of treatment

Project description:We find that TGFβ signaling in SMCs induced ACSS2-dependent production of Ac-CoA in a PDK4-dependent manner. TGFb induces SMC contractile phenotype and glycolysis.

2025-09-01 | GSE288577 | GEO

Effect of Pdk4 smooth muscle cell-specific knockout on atherosclerosis

Project description:Knockout of Pdk4 in smooth muscle cells dramatically decreased inflammation, and increased gene expressions in TGFb signaling and glycolysis in the aorta.

2025-09-01 | GSE288576 | GEO

Effect of Pdk4 smooth muscle cell-specific knockout on atherosclerosis analyzed by scRNAseq

Project description:Knockout of Pdk4 in smooth muscle cells dramatically decreased inflammation, and increased gene expressions in TGFb signaling and glycolysis in the aorta.

2025-09-01 | GSE288834 | GEO

Histone lactylation enhances m6A-mediated PDK4 stabilization to drive osteogenic differentiation in calcific aortic valve disease [RNAseq-PDK4]

Project description:Calcific aortic valvular disease (CAVD) is characterized by progressive thickening and calcification of the valvular leaflets. Emerging evidence suggests that glycolysis, particularly regulated by pyruvate dehydrogenase kinase 4 (PDK4), plays a significant role in calcification-related diseases. Nevertheless, the mechanisms by which PDK4 affects glycolysis and influences CAVD remain unexplored. This study investigated the contribution of PDK4 to glycolytic reprogramming and osteogenic differentiation in CAVD. Osteogenic differentiation of human valvular interstitial cells (VICs) and CAVD valves was associated with enhanced glycolysis, leading to increased lactate production that further promoted VICs' calcification. PDK4 expression was significantly upregulated in both osteogenically differentiated VICs and CAVD valves. Silencing PDK4 reduced osteogenic differentiation in VICs, whereas PDK4 overexpression aggravated differentiation and increased glycolytic activity. Mechanistically, PDK4 facilitated nuclear translocation of Yes-associated protein (YAP), a key regulator of the Hippo signaling pathway, thereby enhancing RUNX2 transcription and promoting osteogenic differentiation. Nuclear accumulation of lactate increased H3K18 lactylation, which stabilized PDK4 mRNA through the METTL3-m6A-YTHDF1 pathway, establishing a positive feedback loop. This study identifies mechanisms by which glycolysis drives CAVD progression and highlights PDK4 as a potential molecular target for therapeutic intervention.

2026-05-01 | GSE309849 | GEO

ACSS2 modulates endothelial glycolysis in angiogenesis

Project description:Endothelial cells (ECs) sustain high glycolytic flux and display remarkable metabolic plasticity. Although the molecular pathways regulating endothelial glycolysis are well characterized, the metabolic mechanisms underlying hypoxia-induced glycolytic activation during angiogenesis remain poorly understood. Here, we show that acetyl-CoA synthetase 2 (ACSS2) serves as a critical metabolic modulator, coupling acetate utilization with glycolytic flux to control EC function and angiogenesis. The high level of ACSS2-mediated acetate-to-acetyl-CoA conversion in angiogenic front ECs sustains acetyl-CoA levels, which are essential for EC proliferation and retinal vascularization. Conversely, endothelial-specific Acss2 deletion disrupts pathological angiogenesis and normalizes tumor vasculature. Mechanistically, ACSS2 maintains hypoxia-inducible factor 1α transcriptional activity and stabilizes glucose transporter 1, thereby preserving glycolysis. Pyruvate dehydrogenase kinase 4 knockdown rescues metabolic and functional defects in ACSS2-deficient ECs, revealing acetyl-CoA homeostasis as a lynchpin of hypoxic endothelial metabolism. Collectively, our work establishes ACSS2 as a pivotal regulator of vascular development and proposes targeting acetate metabolism as a strategy to modulate pathological angiogenesis.

2026-06-01 | GSE301613 | GEO

Effect of PDK4 or ACSS2 knockdown on HASMC phenotype after 7 days of treatment [RNAseq-siPDK4-siACSS2]

Project description:Effect of PDK4 or ACSS2 knockdown on HASMC phenotype after 7 days of treatment [RNAseq-siPDK4-siACSS2]

| PRJNA1219576 | ENA

Acetyl-CoA metabolism by ACSS2 regulates neuronal histone acetylation and long-term memory [RNA-seq]

Project description:Metabolic production of acetyl-CoA has been linked to histone acetylation and gene regulation, however the mechanisms are largely unknown. We show that the metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) is a critical and direct regulator of histone acetylation in neurons and of long-term mammalian memory. We observe increased nuclear ACSS2 in differentiating neurons in vitro. Genome-wide, ACSS2 binding corresponds with increased histone acetylation and gene expression of key neuronal genes. These data indicate that ACSS2 functions as a chromatin-bound co-activator to increase local concentrations of acetyl-CoA and to locally promote histone acetylation for transcription of neuron-specific genes. Remarkably, in vivo attenuation of hippocampal ACSS2 expression in adult mice impairs long-term spatial memory, a cognitive process reliant on histone acetylation. ACSS2 reduction in hippocampus also leads to a defect in upregulation of key neuronal genes involved in memory. These results reveal a unique connection between cellular metabolism and neural plasticity, and establish a link between generation of acetyl-CoA and neuronal chromatin regulation. Global survey of gene expression in CAD cells and differentiated CAD neurons following lentiviral knockdown of ACSS2 or ATP citrate lyase (ACL) (and control = scramble hairpin); survey of hippocampal gene expression changes associated with retrieval of fear memory, after ACSS2-AAV knockdown or in EGFP-AAV control (comparison of 0h vs. 1h post-memory retrieval).

2017-05-01 | E-GEOD-76853 | biostudies-arrayexpress

Histone lactylation enhances m6A-mediated PDK4 stabilization to drive osteogenic differentiation in calcific aortic valve disease

2026-05-01 | GSE309520 | GEO

Expression data from PDK4 overexpressing (Ad-PDK4 infected) and control (Ad-control infected) mouse liver

Project description:We identified PDK4 as a gene with adaptive transcriptional response to chemical stress. Although PDK4 is an energy resource regulator induced by starvation, expression of other fasting-inducible genes was unaffected, indicating additional physiological role of PDK4 for liver adaptation to the chemical stress. We used microarrays to determine genes with altered transcriptional level by PDK4 overexpression. Mice were infected with Ad-control (empty adenovirus vector) or Ad-PDK4 (PDK4 overexpressing adenovirus vector) at a dose of 10^9 PFU/mouse by tail vein injection. 3 days after the infection, mice were sacrificed for RNA preparation from the liver. Ad-control infected = 4, Ad-PDK4 infected = 3. Specimens from mice of each group were pooled, and 10 ug RNA from each pool was used for cRNA synthesis.

2010-12-25 | E-GEOD-22534 | biostudies-arrayexpress

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