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The response of human coronary artery endothelial cells to PPBP treatment

GSE277891 Homo sapiens Expression profiling by high throughput sequencing 8 samples Submitted 2025/06/07 Platform GPL24676
Summary
Pro-platelet basic protein (PPBP), a platelet-derived member of the CXC chemokine family, activates neutrophils and other immune cells via CXCR1 and CXCR2 receptors. It is associated with various diseases, including chronic obstructive pulmonary disease, inflammatory bowel disease, and rheumatoid arthritis. In our study, PPBP was found to be significantly upregulated in both the dermal adipose tissue and plasma of patients with psoriasis. Administration of PPBP or imiquimod in Apoe-/- mice exacerbated atherosclerosis by inducing oxidative stress and mitochondrial dysfunction in coronary artery endothelial cells. Conversely, neutralizing PPBP or administering the mitochondria-targeted antioxidant Mito-TEMPO significantly reduced atherosclerotic plaque formation in these mice. To further explore the mechanisms by which PPBP contributes to atherosclerotic plaque development, we conducted transcriptomic analysis of human coronary artery endothelial cells (HCAEC) treated with PPBP
Published in
Adipose Tissue Macrophage-Derived Proplatelet Basic Protein Exacerbates Psoriasis-Associated Atherosclerosis by Inducing Mitochondrial Dysfunction in Aortic Endothelial Cells
Zhu L, Du L, Wu J et al. · The Journal of investigative dermatology 2026 · PMID 40886963 · doi:10.1016/j.jid.2025.05.041
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Also filed as BioProject PRJNA1164712 and SRA study SRP535748. Searching any of these in the dataset finder brings you back here.

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