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Peritonitis increases MMP-9 activity in peritoneal effluent from CAPD patients.

机译:腹膜炎会增加CAPD患者腹膜排出物中MMP-9的活性。

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Patients undergoing long-term continuous ambulatory peritoneal dialysis (CAPD) sometimes experience ultrafiltration failure. Mesothelial basement membrane thickening and the accumulation of submesothelial fibrotic tissue are common features of the diseased peritoneum. Peritonitis can lead to ultrafiltration failure, but the precise mechanism is not clear. The key enzymes in extracellular matrix (ECM) remodeling, namely matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), are produced by human peritoneal mesothelial cells. Using peritoneal effluent from 13 CAPD patients with peritonitis and 7 noninfected CAPD control individuals, we examined MMP and TIMP activities by gelatin and reverse zymography. Latent and activated types of MMP-2 and -9, and TIMP-1 and -2 were identified in peritoneal effluent (from all CAPD patients). Levels of latent and activated type MMP-9, as well as of TIMP-1 activities were higher at the onset of peritonitis than either during the recovery phase of peritonitis and/ or in control individuals. Activated MMP-9 activity positively correlated with leukocyte numbers and IL-6 levels in peritoneal effluent. Activities of MMP-2 and TIMP-2 in peritoneal effluent did not change between the onset of peritonitis and recovery. We concluded that increased MMP-9 and TIMP-1 levels might be associated with peritoneal ECM remodeling during peritonitis. Copyright 2001 S. Karger AG, Basel
机译:接受长期连续非卧床腹膜透析(CAPD)的患者有时会发生超滤失败。间皮基底膜增厚和间皮下纤维化组织的积累是患病腹膜的常见特征。腹膜炎可导致超滤失败,但确切机制尚不清楚。细胞外基质(ECM)重构中的关键酶,即基质金属蛋白酶(MMP)和组织金属蛋白酶抑制剂(TIMPs),是由人腹膜间皮细胞产生的。使用来自13例腹膜炎的CAPD患者和7例未感染的CAPD对照人群的腹膜流出液,我们通过明胶和反向酶谱法检查了MMP和TIMP活性。在腹膜流出物中(来自所有CAPD患者)鉴定出MMP-2和-9,TIMP-1和-2的潜伏和激活类型。在腹膜炎发作期间,潜伏性和活化型MMP-9的水平以及TIMP-1活性均高于腹膜炎恢复阶段和/或对照组的水平。激活的MMP-9活性与腹膜排出物中的白细胞数目和IL-6水平呈正相关。在腹膜炎发作和恢复之间,MMP-2和TIMP-2在腹膜流出物中的活性没有变化。我们得出结论,腹膜炎期间MMP-9和TIMP-1水平升高可能与腹膜ECM重塑有关。版权所有2001 S. Karger AG,巴塞尔

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