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Dexamethasone, Transforming Growth Factor-β1이 사구체 내피세포의 Vascular Cell Adhesion Molecule-1(VCAM-1) 발현에 미치는 영향 (The Effect of Dexamethasone and Transforming Growth Factor-β1 on the Cytokine Induced Expression of VCAM-1 in Glomerular Endothelial Cells) |
정영옥, 장윤혜, 양원석, 장혜숙, 안한종, 이재담, 박수길, Su Kil Park (Young Ok Jung, Jong Soo Lee, Yoon Hye Chang, Won Seok Yang, Hye Sook Chang, Hanjong Ahn and Jae Dam Lee) |
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Abstract |
Endothelial cell have been shown to play an active role in many phases of immunologic process, including binding of T lymphocytes, neutrophils, platelets, and monocytes to the endothelium, as well as phagocytosis. Endothelial cells can also serve as targets that undergo cell injury. The most prominent mediators of endothelial cell activation are IL-1β and TNF-α. VLA-4 was first identified as an endothelial cell surface receptor. We performed the culture of endothelial cells derived from human glomerular capillaries and studied the cytokine-regulated expression of VCAM- 1 , and the effect of dexamethasone and TGF-β on the cytokine induced VCAM-1 expression using ELISA method.
Expression of VCAM-1 was not detectable above background level in the basal unstimulated state. However, VCAM-1 was rapidly induced after exposure to IL-1β(5ng/ml) or TNF-α(1, 10ng/ml) (O.D.=1.76±0.15, 1.95±0.35, 1.88±0.17, mean±S.E., control=0.36±0.028, n=8-24, P<0.05). But IFN-γdid not increase the expression of VCAM-1. Addition of dexamethasone(10μM) and TGF-β1(1ng, 10ng/ml) blunted IL-1β and TNF-α induced expression of VCAM-1. Therefore, VCAM-1 could be inducible in human glomerular endothelial cells, and it was regulated by dexamethasone and TGF-β1. The negative findings in histopathology may reflect the transience of VCAM-1 expression and does not necessarily exclude an important role of this molecule in the early stages of renal disease. |
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