What is it about?
In this study, we aimed to find key molecules involved in keloid disease (KD) by analyzing the proteins and genes from both normal and KD-affected skin cells. By using advanced techniques, we discovered two specific proteins—NF-kB-p65 (RELA) and CAPN2—that were much more active in KD cells compared to normal ones. These proteins are linked to important processes like cell death (apoptosis), which could help explain why KD scars grow the way they do. We confirmed our findings by further testing these proteins in KD tissue and showed that two medications, omeprazole and dexamethasone, could reduce the growth of KD cells by promoting cell death. These findings may lead to better ways to diagnose and treat keloid disease in the future.
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Why is it important?
What makes this study unique is its use of a label-free shotgun proteomics approach to examine the proteins within different parts of KD fibroblast cells. This technique allows for a more detailed and comprehensive analysis of the molecular biology underlying keloid disease. Additionally, this research focuses on KD samples specifically from people of African ancestry, a population disproportionately affected by the disease. The ethically collected samples from South Africa provide a more relevant insight into how KD develops and progresses in this group. By combining proteomic analysis with validation techniques in actual human tissue, this study identifies and confirms key molecular regulators that could be important for better diagnosis and treatment of KD.
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This page is a summary of: Subcellular Fractionation and Metaproteogenomic Identification and Validation of Key Differentially Expressed Molecular Targets for Keloid Disease, Journal of Investigative Dermatology, August 2024, Elsevier,
DOI: 10.1016/j.jid.2024.07.010.
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