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Transcriptomic profiling of chlorogenic acid and taurine treatment in human skin cells provides insights into cellular senescence mechanisms

ABSTRACT: Chlorogenic acid (CGA) and taurine are well-known antioxidant compounds that have been demonstrated to reduce cellular senescence in the skin. Given their potential synergistic effects, co-treatment with CGA and taurine may enhance their individual efficacy. However, the biological mechanisms underlying their skin-protective effects remain underexplored. This study aimed to identify genes responsive to CGA and taurine and elucidate their anti-senescence-associated pathways. To this end, we conducted transcriptome-wide RNA sequencing to profile gene expression changes of human epidermal keratinocytes, melanocytes, and fibroblasts by treatment of CGA, taurine, and their combination. The differential expression analysis identified 197 differentially expressed genes (DEGs) in response to the compounds, of which 62 were prioritized as aging-related DEGs based on their involvement in skin aging pathways from functional enrichment analysis and supporting evidence from public databases and prior studies. By identifying key genes and pathways that might contribute to the cellular longevity in human skin, this study provides molecular insights for developing anti-aging strategies with potential applications in dermatology.

ORGANISM(S): Homo sapiens

PROVIDER: GSE302932 | GEO | 2026/03/23

REPOSITORIES: GEO

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Project description:Background: Metabolic dysregulation has been implicated in bronchopulmonary dysplasia development. Taurine is an essential amino acid for neonates and is critically involved in glucose and fatty acid metabolism. Neonatal tissue obtains taurine mainly through the taurine transporter. The biological role of taurine in neonatal lung development has never been explored. As glucose metabolism mechanistically modulates angiogenesis and angiogenesis is the central player for neonatal lung development, we hypothesize that taurine depletion contributes to bronchopulmonary dysplasia development. Results: Although most genes and proteins for oxidative phosphorylation were enriched in hyperoxia pup lungs, the complex-1 activity decreased. The decrease in taurine-dependent complex-1 core subunits, ND5 and ND6, in hyperoxia lungs reasonably explained the discrepancy. Metabolomics analysis demonstrated decreased lung taurine with increased blood taurine of hyperoxia pups, compatible with the decreased taurine transporter expression. Decreased glycosylation and increased degradation explained the decreased taurine transporter expression. The results of the complementary study using tunicamycin and tauroursodeoxycholic acid studies supported that endoplasmic reticulum stress contributes to decreased taurine transporter expression in hyperoxia lungs. The effect of taurine treatment on reducing endoplasmic reticulum stress, increasing ND5 and ND6 expression, angiogenesis, and, most importantly, the alveolar formation is beneficial to hyperoxia rat pups. Conclusion: Hyperoxia exposure causes endoplasmic reticulum stress, increases taurine transporter degradation, and leads to taurine depletion in the neonatal lungs with subsequent metabolic dysregulation, resulting in poor alveolar formation of the neonatal lungs. We provide evidence of the never-being-reported protective role of taurine in neonatal lung development. The fact that taurine attenuates the severity of bronchopulmonary dysplasia by reducing hyperoxia-induced endoplasmic reticulum stress and mitochondrial dysfunction indicates its therapeutic potential for treating bronchopulmonary dysplasia.

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Transcriptomic profiling of chlorogenic acid and taurine treatment in human skin cells provides insights into cellular senescence mechanisms

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