| Effect of Uric Acid (UA) on C-reactive Protein (CRP) Expression in Peripheral Blood Mononuclear Cells (PBMC) |
| Duk-Hee Kang, M.D., Mina Yu, M.D. and Jung-Hwa Ryu, M.D. |
| Division of Nephrology, Ewha Womans University College of Medicine, Seoul |
| 원저 : 요산이 말초혈액 단핵세포의 C-반응 단백 (C-reactive protein)의 합성에 미치는 영향 |
| 강덕희 유민아 류정화 |
| 이화여자 대학교 의과대학 내과학교실 |
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| Abstract |
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Purpose : Systemic inflammatory reaction (SIR) is an important determinant of cardiovascular (CV) mortality in CRF patients. UA is an end-product of purine metabolism, and recent studies have demonstrated that an elevated serum UA level is associated with an increased level of inflammatory mediators. Since hyperuricemia is one of the most prevalent complications in CRF and is linked to CV disease, we hypothesized hyperuricemia in CRF may play an important role in the development of
CV disease by inducing SIR.
Methods : PBMCs were isolated by density gradient centrifugation in 21 CRF patients and age and sex-matched 20 healthy adults. CRP expression was evaluated by real time PCR and ELISA in PBMC stimulated with UA (0.3-12 mg/dL).
Results : There was no difference in constitutional CRP expression in PBMC from control and CRF patients. UA induced CRP mRNA (RT-PCR) and protein (ELISA) expression in PBMC, which was blocked by the organic anion transport inhibitor, probenecid (1 mM), suggesting entry of uric acid into cells was responsible for CRP expression. PBMC from CRF patients showed a significantly higher CRP production by UA compared to healthy control. There was no correlation between serum UA level and % increase in CRP production by UA.
Conclusion : The exaggerated CRP expression by UA can be another mechanism of SIR and increased CV morbidity in CRF patients. Prospective studies with uric acid-lowering therapy are necessary to confirm clinical significance of these interesting in-vitro findings.
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| Key Words:
Inflammation, Cardiovascular disease, Uric acid, C-reactive protein |
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