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| 원저 : 신장 혈전성 미세혈관병증 모델에서 미세혈관 회복과 Vascular Endothelial Growth Factor 의 발현 (Recovery of Renal Microvasculature and Expression of VEGF in Experimental Thrombotic Microangiopathy) |
| 김윤구(Yoon Goo Kim),오하영(Ha Young Oh) |
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| Abstract |
Background
: Renal microvascular injury characterizes thrombotic microangiopathy(TMA). In a rat TMA model characterized by progressive renal injury, we postulated that the incomplete resolution of renal injury might be due to inadequate recovery of microvascular endotherlium. We therefore examined the degree of recovery of microvasculature and expression of vascular endothelial growth factor(VEGF), which has trophic, pro-survival, and angiogenic properties for endeothelial cells. Methods: TMA was induced in rats by selective right renal artery perfusion of anti-glomerular endothelial cell IgG(30mg/kg). The rats were studied at day 1 and day 17 and compared with control rats perfused with non-immunized goat IgG. Results: Control rats had normal microvasculature and normal histology at day 1 and day 17. In contrast, rats perfused with anti-GEN(TMA rats) showed severe loss of microvasculature accomapnied by severe glomerular and tubulointerstitial(TI) injury at day l. At day 17 of TMA rats, some spontaneous endothelial recovery was present, but the repair was incomplete and progressive glomerular and TI dam- age occurred. In control rats, VEGF expression was prominent in the outer medulla and medullary rays. In TMA rats, VEGF expresion was markedly decreased compared to control rats at day 1 and the remained decreased at day 17, especially at sites of intersitital fibrosis. Conclusion: Incomplete recovery of renal microvasuclature was associated with severe tissue damage and reduced VEGF expression in a rat model of TMA. These studies suggest that reduced VEGF expression may cause incomplete recovery of injured rena1 microvasulature. and persistent tissue injury |
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