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  4. Anti-CENP-B and anti-TOPO-1-containing sera from systemic sclerosis-related diseases with Raynaud's phenomenon induce vascular endothelial cell senescence not via classical p53-p21 pathway
 
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Anti-CENP-B and anti-TOPO-1-containing sera from systemic sclerosis-related diseases with Raynaud's phenomenon induce vascular endothelial cell senescence not via classical p53-p21 pathway

Journal
Clinical rheumatology
Journal Volume
37
Journal Issue
3
Pages
749
Date Issued
2018-03
Author(s)
CHIEH-YU SHEN  
KO-JEN LI  
Lai, Pei-Hsuan
CHIA-LI YU  
SONG-CHOU HSIEH  
DOI
10.1007/s10067-017-3845-9
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/593953
URL
https://scholars.lib.ntu.edu.tw/handle/123456789/540808
Abstract
Raynaud's phenomenon (RP) is the earliest and most common clinical manifestation in patients with systemic sclerosis (SSc) and its related diseases containing anti-TOPO-1 and/or anti-CENP-B autoantibodies in the sera. However, the cause-effect relationship between the two autoantibodies and RP remains elucidation. Sera containing anti-CENP-B and anti-TOPO-1 autoantibodies were obtained from SSc-related diseases manifesting RP. The polyclonal auto-antibodies were purified from pooled sera by affinity chromatography. Mouse monoclonal anti-CENP-B and anti-TOPO-1 were purchased. Calf pulmonary arterial endothelial cells (CPAE) were incubated with 40% patient sera, purified polyclonal antibodies or mouse monoclonal antibodies for 1-6 days. The vascular endothelial biomarkers von Willebrand factor (vWF), thrombomodulin (CD141) and 6-keto-prostaglandin F1α (6-keto-PGF1α), cell viability marker ATP, and cell necrosis/lysis marker LDH in the culture supernatants were measured by ELISA. The cell senescence biomarker β-galactosidase and telomere content in the cells were stained by the respective kit. The classical p53-p21 senescence pathway was detected by Western blot. We found that 40% anti-CENP-B or anti-TOPO-1-containing sera without heat-inactivation and mouse monoclonal antibodies suppressed 6-keto-PGF1α production, increased β-galactosidase, and decreased relative telomere content. The cell senescence effects were proved not via p53-p21 pathway. The pathognomonic anti-CENP-B and anti-TOPO-1 autoantibodies in SSc-related diseases accelerate vascular endothelial cell senescence and functional impairment inducing RP. The real signaling pathway for autoantibody-induced cell senescence remains exploration.
Subjects
Anti-CENP-B; Anti-TOPO-1; Cell senescence; Raynaud’s phenomenon; Telomere content; p53-p21 pathway; β-galactosidase
SDGs

[SDGs]SDG3

Other Subjects
autoantibody; beta galactosidase; CENP B antibody; lactate dehydrogenase; monoclonal antibody; prostaglandin F1 alpha; protein p21; protein p53; thrombomodulin; TOPO 1 antibody; unclassified drug; von Willebrand factor; 6 oxoprostaglandin F1 alpha; autoantibody; centromere protein B; DNA topoisomerase; thrombomodulin; von Willebrand factor; affinity chromatography; animal cell; Article; cell viability; controlled study; endothelial cell line; nonhuman; priority journal; pulmonary artery; Raynaud phenomenon; senescence; systemic sclerosis; telomere; animal; blood; bovine; cell aging; cell line; endothelium cell; human; immunology; metabolism; signal transduction; vascular endothelium; 6-Ketoprostaglandin F1 alpha; Animals; Autoantibodies; Cattle; Cell Line; Cellular Senescence; Centromere Protein B; DNA Topoisomerases, Type I; Endothelial Cells; Endothelium, Vascular; Humans; Raynaud Disease; Scleroderma, Systemic; Signal Transduction; Thrombomodulin; von Willebrand Factor
Publisher
SPRINGER LONDON LTD
Type
journal article

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