scholarly journals Elevated plasma asymmetric dimethyl-L-arginine levels are linked to endothelial progenitor cell depletion and carotid atherosclerosis in rheumatoid arthritis

2007 ◽  
Vol 56 (3) ◽  
pp. 809-819 ◽  
Author(s):  
Andrzej Surdacki ◽  
Jens Martens-Lobenhoffer ◽  
Alicja Wloch ◽  
Ewa Marewicz ◽  
Tomasz Rakowski ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Carotid Atherosclerosis ◽  
Cell Depletion ◽  
Elevated Plasma ◽  
Endothelial Progenitor

Red cell distribution width is associated with endothelial progenitor cell depletion and vascular-related mediators in rheumatoid arthritis

2015 ◽  
Vol 240 (1) ◽  
pp. 131-136 ◽  
Author(s):  
Javier Rodríguez-Carrio ◽  
Mercedes Alperi-López ◽  
Patricia López ◽  
Sara Alonso-Castro ◽  
Santiago Rubén Carro-Esteban ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Red Cell Distribution Width ◽  
Cell Depletion ◽  
Red Cell ◽  
Cell Distribution ◽  
Endothelial Progenitor ◽  
Distribution Width

scholarly journals CXCL13/CXCR5 axis facilitates endothelial progenitor cell homing and angiogenesis during rheumatoid arthritis progression

2021 ◽  
Vol 12 (9) ◽  
Author(s):  
Chun-Hao Tsai ◽  
Chao-Ju Chen ◽  
Chi-Li Gong ◽  
Shan-Chi Liu ◽  
Po-Chun Chen ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Vascular Endothelial ◽  
Cellular Functions ◽  
Endothelial Progenitor ◽  
Ankle Joints ◽  
Cartilage Erosion ◽  
Endothelial Growth Factor

AbstractAngiogenesis is a critical process in the formation of new capillaries and a key participant in rheumatoid arthritis (RA) pathogenesis. The chemokine (C-X-C motif) ligand 13 (CXCL13) plays important roles in several cellular functions such as infiltration, migration, and motility. We report significantly higher levels of CXCL13 expression in collagen-induced arthritis (CIA) mice compared with controls and also in synovial fluid from RA patients compared with human osteoarthritis (OA) samples. RA synovial fluid increased endothelial progenitor cell (EPC) homing and angiogenesis, which was blocked by the CXCL13 antibody. By interacting with the CXCR5 receptor, CXCL13 facilitated vascular endothelial growth factor (VEGF) expression and angiogenesis in EPC through the PLC, MEK, and AP-1 signaling pathways. Importantly, infection with CXCL13 short hairpin RNA (shRNA) mitigated EPC homing and angiogenesis, articular swelling, and cartilage erosion in ankle joints of mice with CIA. CXCL13 is therefore a novel therapeutic target for RA.

scholarly journals Apelin Promotes Endothelial Progenitor Cell Angiogenesis in Rheumatoid Arthritis Disease via the miR-525-5p/Angiopoietin-1 Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Ting-Kuo Chang ◽  
You-Han Zhong ◽  
Shan-Chi Liu ◽  
Chien-Chung Huang ◽  
Chun-Hao Tsai ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Synovial Fibroblasts ◽  
Tube Formation ◽  
Endothelial Progenitor ◽  
Rheumatoid Arthritis Disease ◽  
Cartilage Erosion ◽  
And Migration ◽  
Angiopoietin 1

Angiogenesis is a critical process in the formation of new capillaries and a key participant in rheumatoid arthritis (RA) pathogenesis. The adipokine apelin (APLN) plays critical roles in several cellular functions, including angiogenesis. We report that APLN treatment of RA synovial fibroblasts (RASFs) increased angiopoietin-1 (Ang1) expression. Ang1 antibody abolished endothelial progenitor cell (EPC) tube formation and migration in conditioned medium from APLN-treated RASFs. We also found significantly higher levels of APLN and Ang1 expression in synovial fluid from RA patients compared with those with osteoarthritis. APLN facilitated Ang1-dependent EPC angiogenesis by inhibiting miR-525-5p synthesis via phospholipase C gamma (PLCγ) and protein kinase C alpha (PKCα) signaling. Importantly, infection with APLN shRNA mitigated EPC angiogenesis, articular swelling, and cartilage erosion in ankle joints of mice with collagen-induced arthritis. APLN is therefore a novel therapeutic target for RA.

scholarly journals Endothelial Progenitor Cell (EPC) Recruitment in Rheumatoid Arthritis

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Matthew David Silverman ◽  
Christian S Haas ◽  
Ali M Rad ◽  
Ali S Arbab ◽  
Alisa E Koch
Keyword(s):  
Rheumatoid Arthritis ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Endothelial Progenitor

scholarly journals Enhanced late-outgrowth circulating endothelial progenitor cell levels in rheumatoid arthritis and correlation with disease activity

2010 ◽  
Vol 12 (1) ◽  
pp. R27 ◽  
Author(s):  
Vanina Jodon de Villeroché ◽  
Jérome Avouac ◽  
Aurélie Ponceau ◽  
Barbara Ruiz ◽  
André Kahan ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Disease Activity ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Endothelial Progenitor

scholarly journals Adiponectin Promotes VEGF Expression in Rheumatoid Arthritis Synovial Fibroblasts and Induces Endothelial Progenitor Cell Angiogenesis by Inhibiting miR-106a-5p

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2627
Author(s):  
Chien-Chung Huang ◽  
Yat-Yin Law ◽  
Shan-Chi Liu ◽  
Sung-Lin Hu ◽  
Jun-An Lin ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Therapeutic Potential ◽  
Joint Destruction ◽  
Bone Destruction ◽  
Synovial Cell ◽  
Vegf Expression ◽  
Endothelial Progenitor

Rheumatoid arthritis (RA) is an erosive polyarthritis that can lead to severe joint destruction and painful disability if left untreated. Angiogenesis, a critical pathogenic mechanism in RA, attracts inflammatory leukocytes into the synovium, which promotes production of proinflammatory cytokines and destructive proteases. Adipokines, inflammatory mediators secreted by adipose tissue, also contribute to the pathophysiology of RA. The most abundant serum adipokine is adiponectin, which demonstrates proinflammatory effects in RA, although the mechanisms linking adiponectin and angiogenic manifestations of RA are not well understood. Our investigations with the human MH7A synovial cell line have revealed that adiponectin dose- and time-dependently increases vascular endothelial growth factor (VEGF) expression, stimulating endothelial progenitor cell (EPC) tube formation and migration. These adiponectin-induced angiogenic activities were facilitated by MEK/ERK signaling. In vivo experiments confirmed adiponectin-induced downregulation of microRNA-106a-5p (miR-106a-5p). Inhibiting adiponectin reduced joint swelling, bone destruction, and angiogenic marker expression in collagen-induced arthritis (CIA) mice. Our evidence suggests that targeting adiponectin has therapeutic potential for patients with RA. Clinical investigations are needed.

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