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Blood, Vol. 108, Issue 6, 1849-1856, September 15, 2006
Signaling of vascular endothelial growth factor receptor-1 tyrosine kinase promotes rheumatoid arthritis through activation of monocytes/macrophages
Blood Murakami et al.
108: 1849
Supplemental materials for: Murakami et al
Files in this Data Supplement:
- Table S1. List of 60 polymorphism markers. (PCR-SSLP marker) (PDF, 56.9 KB)
- Table S2. Primers for PT-PCR analysis of gene expression (PDF, 41.5 KB)
- Figure S1. Effect of KRN951 on the VEGF-A-induced phosphorylation of the tyrosine kinase of VEGFR-1 and VEGFR-2 expressed in NIH3T3 cells (JPG, 37.9 KB)
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A low molecular weight chemical, KRN951, blocked the phosphorylation of the tyrosine kinase of VEGFR-1 and VEGFR-2 induced by VEGF-A in NIH3T3 cells. Serum-starved VEGFR-1- and VEGFR-2-NIH3T3 cells were treated with KRN951 (100nM) for 1 hour before being stimulated with VEGF-A (50 ng/ml). The cells were then lysed and the lysates were subjected to SDS-PAGE and immunoblotting with anti–VEGFR-1, anti-VEGFR-2, anti-PY20 and anti-phospho-PLC antibodies.
- Figure S2. Total amounts of angiogenic factors and Pro-inflammatory factors in the joints are significantly increased as determined by Real-time RT-PCR analysis (JPG, 47.5 KB)
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Inflamed synovial tissues within the joints were resected from wild-type mice (no arthritis) and mice with pX-induced arthritis (severe arthritis) under a microscope. A Real-time RT-PCR analysis of angiogenic factors and pro-inflammatory cytokines was performed with total RNA. (A-B) mRNA expression of angiogenic factors and pro-inflammatory cytokines in arthritic joints was significantly increased compared with that in normal wild-type joints. The data represent the mean ± s.e.m. *, p<0.05, **, p<0.01.
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