Analysis of expression and its clinical significance of the ADAMTS-2 in systemic lupus erythematosus

Objectives: ADAMTS-2 is a procollagen N-proteinase that plays an important role in inflammation regulation. The objective of our research is to explore the expression of ADAMTS-2 in Systemic Lupus Erythematosus (SLE), and analyze its relationship with clinical features of SLE, and evaluate the potential value of ADAMTS-2 as a diagnostic biomarker in SLE.

Methods: ADAMTS-2 expression in PBMCs was detected by RT-qPCR in SLE patients, RA patients, and healthy controls (HC). The diagnostic value of ADAMTS-2 for SLE was evaluated by ROC curve, and the correlation between ADAMTS-2 and the clinical characteristics of SLE was analyzed by Spearman's rank correlation coefficient. The expression profiles of GSE8650 and GSE82221 were downloaded from the GEO database. We performed GSEA to further understand the functions of ADAMTS-2 in SLE. CIBERSORT was utilized for immune cell infiltration analysis.

Results: RT-qPCR results validated that the expression of ADAMTS-2 in PBMCs was significantly increased in SLE patients than RA patients and HC. ROC anaylsis suggested that ADAMTS-2 has significant value in distinguishing new-onset SLE patients from RA patients and HC (AUC = 0.805, p < 0.0001). The expression of ADAMTS-2 was negatively correlated with C3, WBC, PLT, neutrophil, and monocyte level. PBMCs samples with high ADAMTS-2 expression were enriched in TNFA_SIGNALING_VIA_NFKB pathway. We found that ADAMTS-2 was positively correlated with neutrophils, M0 macrophages and M2 macrophages.

Conclusion: ADAMTS-2 may be a potential biomarker of SLE patients and closely related to the occurrence and development of SLE. ADAMTS-2 is expected to be a new target for SLE treatment. Key Points • ADAMTS-2 is a potential biomarker of disease activity in SLE patients that develop a flare. • Samples with high ADAMTS-2 expression are enriched in TNFA_SIGNALING_VIA_NFKB pathway in SLE. • ADAMTS-2 expression is positively correlated with neutrophils, M0 macrophages and M2 macrophages.