The response of human coronary artery endothelial cells to PPBP treatment

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 HCAECs were treating with PPBP protein. The total RNA was isolated for subsequent RNA sequencing analysis.