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凝集素在体外诱导的微血管对胶体碳通透性增加可能涉及蛋白激酶C的激活。

Lectin-induced increase in microvascular permeability to colloidal carbon in vitro may involve protein kinase C activation.

作者信息

Northover A M, Northover B J

机构信息

Department of Pharmacy, School of Applied Sciences, De Montfort University, Leicester, UK.

出版信息

Agents Actions. 1994 May;41(3-4):136-9. doi: 10.1007/BF02001906.

DOI:10.1007/BF02001906
PMID:7942320
Abstract

Two plant lectins, wheat germ agglutinin (WGA) and concanavalin A (Con A), which are known to bind to endothelial cells (ECs), were found to increase the leakage of colloidal carbon (CC) into the walls of microvessels in the villi of rat small intestine, when added to a gelatin-containing perfusate (GPSS) at a concentration of 10 micrograms/ml. Pretreatment of the microvessels with the protein kinase C (PKC) inhibitor Ro 31-8220 (1 x 10(-6) M) significantly reduced this effect. In contrast, the leakage of CC in response to A23187 (1 x 10(-4) M) was not affected by Ro 31-8220. Peanut agglutinin (PNA) and succinyl concanavalin A (SuccCon A), which do not bind to ECs, had no effect at a concentration of 10 micrograms/ml. A lower concentration of WGA (1 microgram/ml) had no significant effect of its own, but significantly reduced the leakage of CC in response to both platelet-activating factor (PAF, 5 x 10(-6) M) and 5-hydroxytryptamine (5-HT, 1 x 10(-4) M), but not to beta-phorbol 12,13-dibutyrate (PDB, 1 x 10(-6) M). These results suggest that all these effects of WGA and Con A involve cell surface receptors, albeit in a non-specific way. A possible mode of action is discussed.

摘要

已知两种植物凝集素,即麦胚凝集素(WGA)和伴刀豆球蛋白A(Con A)可与内皮细胞(EC)结合,当以10微克/毫升的浓度添加到含明胶的灌注液(GPSS)中时,它们会增加大鼠小肠绒毛微血管壁中胶体碳(CC)的渗漏。用蛋白激酶C(PKC)抑制剂Ro 31-8220(1×10⁻⁶ M)对微血管进行预处理可显著降低这种作用。相比之下,Ro 31-8220对A23187(1×10⁻⁴ M)引起的CC渗漏没有影响。不与EC结合的花生凝集素(PNA)和琥珀酰伴刀豆球蛋白A(SuccCon A)在10微克/毫升的浓度下没有作用。较低浓度的WGA(1微克/毫升)本身没有显著作用,但可显著降低血小板活化因子(PAF,5×10⁻⁶ M)和5-羟色胺(5-HT,1×10⁻⁴ M)引起的CC渗漏,但对β-佛波醇12,13-二丁酸酯(PDB,1×10⁻⁶ M)引起的CC渗漏没有影响。这些结果表明,WGA和Con A的所有这些作用都涉及细胞表面受体,尽管方式是非特异性的。文中讨论了一种可能的作用模式。

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本文引用的文献

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Identification of a tumor-specific determinant on neoplastic cell surfaces.肿瘤细胞表面肿瘤特异性决定簇的鉴定。
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Stimulation of protein kinase C activity may increase microvascular permeability to colloidal carbon via alpha-isoenzyme.蛋白激酶C活性的刺激可能通过α同工酶增加微血管对胶体碳的通透性。
Inflammation. 1994 Oct;18(5):481-7. doi: 10.1007/BF01560695.
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Vasoconstriction in rat isolated mesentery and small intestine in response to various activators of protein kinase C.大鼠离体肠系膜和小肠对蛋白激酶C各种激活剂的血管收缩反应。
Agents Actions. 1994 Nov;43(1-2):29-34. doi: 10.1007/BF02005760.
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Involvement of protein kinase C in the control of microvascular permeability to colloidal carbon.蛋白激酶C参与对微血管对胶体碳通透性的调控。
Agents Actions. 1993 Jul;39(3-4):132-6. doi: 10.1007/BF01998965.
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