ArticleBMC molecular biology2016
Stearoyl-CoA desaturase 1 expression is downregulated in liver and udder during E. coli mastitis through enhanced expression of repressive C/EBP factors and reduced expression of the inducer SREBP1A.
Article in BMC molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Cytokine interactions and chemokine dysregulations in mastitis immunopathogenesis: insights from transcriptomic profiling of milk somatic cells in tropical Sahiwal (Frontiers in immunology · 2025Article
- SNP Analysis of TLR4 Promoter and Its Transcriptional Factor Binding Profile in Relevance to Bovine Subclinical Mastitis.Biochemical genetics · 2024Article
- Lactobacillus plantarum 17-5 attenuates Escherichia coli-induced inflammatory responses via inhibiting the activation of the NF-κB and MAPK signalling pathways in bovine mammary epithelial cells.BMC veterinary research · 2022Article
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- The Role of Promoter-Associated Histone Acetylation ofFrontiers in plant science · 2018Article
- Tissue-specific insulin signaling mediates female sexual attractiveness.PLoS genetics · 2017Article
- Is the FVB/N mouse strain truly resistant to diet-induced obesity?Physiological reports · 2017Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
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Abstract
backgroundStearoyl-CoA desaturase 1 (SCD1) desaturates long chain fatty acids and is therefore a key enzyme in fat catabolism. Its synthesis is downregulated in liver during illnesses caused by high levels of circulating lipopolysaccharide (LPS). SCD1 expression is known to be stimulated under adipogenic conditions through a variety of transcription factors, notably SREBP1 and C/EBPα and -β. However, mechanisms downregulating SCD1 expression during illness related reprograming of the metabolism were unknown. Escherichia coli elicited mastitis is an example of such a condition and was found to downregulates milk and milk fat synthesis. This is in part mediated through epigenetic mechanisms. We analyzed here mechanism controlling SCD1 expression in livers and udders from cows suffering from experimentally induced E. coli mastitis.
resultsWe validated with RT-qPCR that SCD1 expression was reduced in these organs of the experimental cows. They also featured decreased levels of mRNAs encoding SREBP1a but increased levels for C/EBP α and -β. Chromatin accessibility PCR (CHART) revealed that downregulation of SCD1 expression in liver was not caused by tighter chromatin compaction of the SCD1 promoter. Reporter gene analyses showed in liver (HepG2) and mammary epithelial (MAC-T) model cells that overexpression of SREBP1a expectedly activated the promoter, while unexpectedly C/EBPα and -β strongly quenched the promoter activity. Abrogation of two from among of the three C/EBP DNA-binding motifs of the promoter revealed that C/EBPα acts in cis but C/EBPβ in trans. Overexpressing truncated C/EBPα or -β factors lacking their repressive domains confirmed in both model cells the direct action of C/EBPα, but not of C/EBPβ on the promoter.
conclusionsWe found no evidence that epigenetic mechanism remodeling the chromatin compaction of the SCD1 promoter would contribute to downregulate SCD1 expression during infection. Instead, our data show for the first time that C/EBP factors may repress SCD1 expression in liver and udder rather than stimulating as it was previously shown in adipocytes. This cell type specific dual and opposite function of C/EBP factors for regulating SCD1 expression was previously unknown. Infection related activation of their expression combined with downregulated expression of SREBP1a explains reduced SCD1 expression in liver and udder during acute mastitis.
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