Decreased serum thrombospondin-1 and elevation of its autoantibody are associated with multiple exacerbated clinical manifestations in systemic lupus erythematosus

Clinical Rheumatology
Yang MengXiaolin Sun

Abstract

The pathological effects of thrombospondin-1 (TSP-1) have been studied in many preclinical tumor models and rheumatoid arthritis. However, the role of TSP-1 and anti-thrombospondin-1 autoantibodies (ATSA) in systemic lupus erythematosus (SLE) has not been specifically defined. In this study, we investigated the clinical relevance and functional significance of TSP-1 and ATSA in SLE patients. Serum levels of TSP-1 and ATSA were measured by ELISA in 138 adult SLE patients and 60 healthy controls. Blood cell counts, rheumatoid factor (RF), immunoglobulins, erythrocyte sedimentation rate (ESR), complements, and SLE-related autoantibodies were measured by standard laboratory techniques. Disease activity was assessed by systemic lupus erythematosus disease activity index (SLEDAI). TSP-1 concentrations were significantly lower in SLE patients compared with those in healthy controls. A significant difference of TSP-1 was observed in the patients with serositis, C3 decrease, RF positive, leukocytopenia, and thrombocytopenia. The levels of TSP-1 showed a positive correlation with the number of leukocyte and thrombocyte, while a negative correlation with anti-dsDNA antibody, IgG, ESR, and SLEDAI. ATSA was observed in 58.7% (81/138) of SLE...Continue Reading

References

Apr 1, 1985·The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society·T N WightP Bornstein
Mar 31, 1995·The Journal of Biological Chemistry·S Schultz-CherryJ E Murphy-Ullrich
Jul 10, 1998·Cell·S E CrawfordN Bouck
Aug 18, 2001·The Journal of Immunology : Official Journal of the American Association of Immunologists·M N AviceM Sarfati
Oct 22, 2003·The Journal of Experimental Medicine·Virginie DoyenMarika Sarfati
Apr 20, 2004·The International Journal of Biochemistry & Cell Biology·Svetlana A Kuznetsova, David D Roberts
Sep 3, 2004·The Journal of Biological Chemistry·Geoffrey D Young, Joanne E Murphy-Ullrich
Mar 17, 2006·Free Radical Biology & Medicine·Jeff S IsenbergMichael Graham Espey
Jul 13, 2006·The Journal of Biological Chemistry·Jeff S IsenbergDavid D Roberts
Sep 5, 2006·The Journal of Immunology : Official Journal of the American Association of Immunologists·Philippe GrimbertMarika Sarfati
Jan 15, 2008·Cellular and Molecular Life Sciences : CMLS·J S IsenbergD D Roberts
Oct 16, 2008·Current Drug Targets·Marika SarfatiSantos Susin
Jul 19, 2011·Mediators of Inflammation·Zenaida Lopez-DeeLinda S Gutierrez
Jun 9, 2012·Annals of the Rheumatic Diseases·Kaname OhyamaNaotaka Kuroda
Aug 8, 2012·Nature Reviews. Rheumatology·Eric BoilardPeter A Nigrovic
Sep 14, 2012·The Journal of Immunology : Official Journal of the American Association of Immunologists·Rajalakshmy RamalingamPawel R Kiela
Mar 21, 2015·PloS One·Laura Contreras-Ruiz, Sharmila Masli
Apr 18, 2015·International Journal of Rheumatic Diseases·Ju-Yang Jung, Chang-Hee Suh
May 12, 2015·The Journal of Clinical Investigation·Vaishali R Moulton, George C Tsokos

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Citations

Dec 4, 2020·International Journal of Molecular Sciences·Sharmila Masli, Darlene A Dartt
Oct 16, 2020·Arthritis Research & Therapy·Michal A RahatDevy Zisman

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