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层粘连蛋白在体外介导大鼠胃黏膜的修复。

Laminin mediates the restitution of rat gastric mucosa in vitro.

作者信息

Miller M A, Bunnett N W, Debas H T

机构信息

Department of Surgery, University of California, San Francisco 94143-0660.

出版信息

Exp Physiol. 1994 Sep;79(5):647-59. doi: 10.1113/expphysiol.1994.sp003797.

Abstract

Restitution, the rapid re-establishment of mucosal integrity following damage, involves cell migration and can be monitored by measuring transmucosal potential difference of tissue mounted in an Ussing chamber. The involvement of extracellular matrix proteins and matrix receptors was examined in the restitution of rat gastric mucosa. Undamaged mucosa maintained a potential difference of -32.7 +/- 2.2 mV for several hours. Mucosal exposure to 0.6 M NaCl for 1 min reduced this to -3.3 +/- 1.4 mV in 2-3 min. Thereafter, the potential difference returned in 60 min to plateau at -28.9 +/- 1.3 mV (88.5 +/- 3.6% of pre-exposure). Tissues mucosally treated with 1:100 anti-laminin antiserum maximally recovered following damage to 65.6 +/- 6.6% of pre-exposure potential difference (PD), while those treated with 1:100 anti-collagen IV or anti-fibronectin antisera recovered to 88.8 +/- 9.7% and 86.3 +/- 3.2%, respectively. Only the anti-laminin result was significantly different from controls. The anti-laminin effect was abolished by pre-incubation of the anti-laminin antiserum with purified rat laminin, suggesting that the effect was laminin specific. In experiments involving matrix protein receptors, tissues treated with alpha-lactalbumin, a protein altering the substrate specificity of cell surface laminin receptor/enzyme beta-1,4-galactosyltransferase, maximally recovered following damage to only 49.3 +/- 7.7% of pre-exposure PD, which was significantly different from controls, while those treated with anti-beta 1 integrin recovered to 85.0 +/- 9.7%. Our data suggest that laminin is involved in mediation of gastric mucosal restitution, possibly via beta-1,4-galactosyltransferase.

摘要

修复是指在损伤后黏膜完整性的快速重建,涉及细胞迁移,可通过测量置于尤斯灌流小室中的组织的跨黏膜电位差来监测。本研究检测了细胞外基质蛋白和基质受体在大鼠胃黏膜修复中的作用。未受损的黏膜在数小时内维持-32.7±2.2 mV的电位差。黏膜暴露于0.6 M NaCl 1分钟后,在2-3分钟内将其降至-3.3±1.4 mV。此后,电位差在60分钟内恢复,稳定在-28.9±1.3 mV(损伤前的88.5±3.6%)。用1:100抗层粘连蛋白抗血清进行黏膜处理的组织,损伤后最大恢复至损伤前电位差(PD)的65.6±6.6%,而用1:100抗IV型胶原或抗纤连蛋白抗血清处理的组织分别恢复至88.8±9.7%和86.3±3.2%。只有抗层粘连蛋白的结果与对照组有显著差异。抗层粘连蛋白抗血清与纯化的大鼠层粘连蛋白预孵育后,其抗层粘连蛋白作用被消除,表明该作用具有层粘连蛋白特异性。在涉及基质蛋白受体的实验中,用α-乳白蛋白处理的组织,α-乳白蛋白是一种改变细胞表面层粘连蛋白受体/酶β-1,4-半乳糖基转移酶底物特异性的蛋白质,损伤后最大恢复至损伤前PD的49.3±7.7%,与对照组有显著差异,而用抗β1整合素处理的组织恢复至85.0±9.7%。我们的数据表明,层粘连蛋白可能通过β-1,4-半乳糖基转移酶参与胃黏膜修复的介导过程。

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