Abstract: Objective To investigate the expression of dermatopontin (DPT) in abdominal aortic aneurysm (AAA) and to explore the mechanism in promoting AAA progression. Methods Differential gene expression (DEG) and GO-KEGG pathway enrichment were used to assess DPT expression level and related pathways in AAA. AAA tissue samples were collected from patients undergoing open surgical repair at Beijing Hospital (experimental group, n=3), while control aortic tissues were collected from kidney transplant donors (n=3). Immun-ohistochemistry and immuno-fluorescence staining were performed to validate DPT protein expression differences in AAA tissues. Masson staining microscopy was used to evaluate fibrosis level. Human aortic smooth muscle cells (HASMCs) were divided into control (Ctrl) and lipopolysaccharide (LPS)-treated groups (n=3). RT-qPCR, ELISA, and immunocytochemistry (ICC) were used to measure DPT expression level. HASMCs were further divided into control (Ctrl) and recombinant human DPT-treated groups with 3 cases in each. RT-qPCR was performed to detect the expression of interleukin-1α (IL-1α), interleukin-1β(IL-1β), collagen type Ⅰ alpha 1 chain (COL1A1), matrix metalloproteinase-2(MMP2), and matrix metalloproteinase-9(MMP9). Cell adhesion assays were conducted to examine the role of integrin α3 and integrin β1 in HASMC adhesion. Results DPT was highly expressed in human AAA tissues (P＜0.01). LPS induced DPT expression and secretion in HASMCs (P＜0.05). DPT promoted IL-1α (P＜0.001) and IL-1β (P＜0.01) expression through a positive feedback mechanism while suppressed COL1A1 (P＜0.001) production. DPT enhanced HASMC adhesion via the integrin α3β1 receptor (P＜0.001). Conclusions DPT promotes AAA progression by activating IL-1α/IL-1β inflammatory cytokines and inhibits COL1A1-mediated extra cellular matrix (ECM) remodeling.Integrin α3β1 is potentially involved in the regulation process.

Key words: abdominal aortic aneurysm, dermatopontin, inflammatory response, extracellular matrix remodeling, smooth muscle cell