Genes & genomics · 2026
Transcriptomic profiling suggests restoration of epidermal barrier-associated lipid metabolism in Egr1-deficient skin following house dust mite exposure.
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Jung Euitaek, Choi Yena, Kang HeeWon, Shin Soon Young
Аннотация
BACKGROUND: House dust mite (HDM) is a major environmental allergen that promotes cutaneous inflammation and disrupts epidermal barrier-associated processes. Early growth response 1 (EGR1) is an inducible transcription factor implicated in inflammatory skin responses; however, its relationship with epidermal barrier-associated lipid metabolism during allergen exposure remains poorly understood.
OBJECTIVE: This study investigated whether Egr1 deficiency is associated with preservation of epidermal barrier-related features and restoration of lipid metabolic transcriptional programs following HDM exposure.
METHODS: Epidermal alterations and filaggrin (FLG) expression were evaluated in wild-type (WT) and Egr1-knockout (KO) mice following topical HDM exposure. A previously generated RNA-seq dataset from WT and Egr1-KO skin with or without HDM treatment was reanalyzed as an exploratory transcriptomic dataset. Expression-change profiling, functional enrichment, and gene set enrichment analyses were used to identify HDM-responsive transcriptional patterns associated with Egr1 deficiency. Selected lipid metabolism-associated genes were independently examined by quantitative real-time PCR.
RESULTS: HDM exposure induced epidermal abnormalities and markedly reduced FLG expression in WT mice, whereas these changes were attenuated in Egr1-KO mice. Exploratory transcriptomic profiling suggested that Egr1 deficiency reprogrammed, rather than globally suppressed, the transcriptional response to HDM. Genes suppressed by HDM but restored in Egr1-deficient skin were preferentially associated with lipid metabolic processes, including fatty acid and sphingolipid metabolism. Gene set enrichment analysis further showed reciprocal enrichment of several lipid-related pathways between WT-HDM versus WT-control and KO-HDM versus WT-HDM comparisons. Independent expression analysis supported the recovery of Elovl6, Hacd2, and Cidec in HDM-treated Egr1-KO skin.
CONCLUSION: Egr1 deficiency is associated with attenuation of HDM-induced FLG loss and restoration of selected epidermal lipid metabolism-associated transcriptional patterns. These findings suggest that EGR1-associated inflammatory responses may intersect with epidermal lipid metabolism during allergen exposure and provide a basis for further investigation of EGR1 in the inflammation-barrier interface.
OBJECTIVE: This study investigated whether Egr1 deficiency is associated with preservation of epidermal barrier-related features and restoration of lipid metabolic transcriptional programs following HDM exposure.
METHODS: Epidermal alterations and filaggrin (FLG) expression were evaluated in wild-type (WT) and Egr1-knockout (KO) mice following topical HDM exposure. A previously generated RNA-seq dataset from WT and Egr1-KO skin with or without HDM treatment was reanalyzed as an exploratory transcriptomic dataset. Expression-change profiling, functional enrichment, and gene set enrichment analyses were used to identify HDM-responsive transcriptional patterns associated with Egr1 deficiency. Selected lipid metabolism-associated genes were independently examined by quantitative real-time PCR.
RESULTS: HDM exposure induced epidermal abnormalities and markedly reduced FLG expression in WT mice, whereas these changes were attenuated in Egr1-KO mice. Exploratory transcriptomic profiling suggested that Egr1 deficiency reprogrammed, rather than globally suppressed, the transcriptional response to HDM. Genes suppressed by HDM but restored in Egr1-deficient skin were preferentially associated with lipid metabolic processes, including fatty acid and sphingolipid metabolism. Gene set enrichment analysis further showed reciprocal enrichment of several lipid-related pathways between WT-HDM versus WT-control and KO-HDM versus WT-HDM comparisons. Independent expression analysis supported the recovery of Elovl6, Hacd2, and Cidec in HDM-treated Egr1-KO skin.
CONCLUSION: Egr1 deficiency is associated with attenuation of HDM-induced FLG loss and restoration of selected epidermal lipid metabolism-associated transcriptional patterns. These findings suggest that EGR1-associated inflammatory responses may intersect with epidermal lipid metabolism during allergen exposure and provide a basis for further investigation of EGR1 in the inflammation-barrier interface.