Slit2 is a potential biomarker for renal impairment in systemic lupus erythematosus
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ORIGINAL ARTICLE
Slit2 is a potential biomarker for renal impairment in systemic lupus erythematosus Yi Zhang1,2 · Lingzhen Hu1 · Xiang Li3 · Liheng Chen1 · Xuyan Yang1 Received: 30 March 2020 / Accepted: 14 September 2020 © Springer Nature Switzerland AG 2020
Abstract Slit2 glycoprotein has been described to regulate the inflammatory response and be involved in autoimmune diseases. Here, we investigated the expression of Slit2 and its potential significance in systemic lupus erythematosus (SLE). A total of 103 patients with SLE participated in our study. The levels of serum Slit2 were measured by enzyme-linked immunosorbent assay, and the expression of Slit2 in renal tissue was detected by immunohistochemistry. Patients with active disease had higher levels of serum Slit2 than patients with inactive disease and controls. Patients with sole skin impairment or sole renal impairment or both skin and renal impairment had higher levels of serum Slit2 than patients with neither skin nor renal impairment. Patients with chronic kidney disease (CKD) had higher levels of serum Slit2 than patients with no CKD. Levels of serum Slit2 in patients with active disease were positively correlated with the SLE Disease Activity Index, complement C4, and anti-dsDNA antibody. Levels of serum Slit2 in patients with CKD were positively correlated with serum creatinine, urine protein, and glomerular filtration rate. The expression of Slit2 and its receptor Roundabout1 (Robo1) in the renal tissue of patients with lupus nephritis were higher than controls. Moreover, renal Slit2 was positively correlated with renal chronic index. Our data indicated that Slit2 may contribute to renal impairment and this may be a potential biomarker for SLE. Keywords Systemic lupus erythematosus (SLE) · Lupus nephritis (LN) · Slit2 · Disease severity
Introduction Systemic lupus erythematosus (SLE), defined as a complex and chronic inflammatory autoimmune disease that can affect many organs.[1–6]. For advances in our understanding of disease pathogenesis and drug development, the prognosis for SLE patients has been greatly improved [7–9], however, patients with SLE still have a 3- to fivefold increased
Yi Zhang, Lingzhen Hu have contributed equally to this work and should be considered co-first authors. * Xuyan Yang [email protected] 1
Department of Rheumatology, Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310009, People’s Republic of China
2
Department of Medicine, Hangzhou Dingqiao Hospital, Hangzhou 310021, People’s Republic of China
3
Clinical Laboratory, Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310009, People’s Republic of China
mortality compared with the general population [2], and the exact etiology of SLE remains unclear. Slit2, as a member of the Slit family, is secreted glycoprotein initially described as an axonal repellent in the developing central nervous system (CNS) [10, 11]. Slit2 functions by binding to its transmembrane receptor Robo. Robo has f
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