A protein kinase C agonist, selective for the beta I isozyme, induces E-selectin and VCAM-1 expression on HUVEC but does not translocate PKC.

A protein kinase C agonist, selective for the beta I isozyme, induces E-selectin and VCAM-1 expression on HUVEC but does not translocate PKC.
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蛋白激酶 C 激动剂对 β I 同工酶具有选择性,可诱导 HUVEC 上的 E-选择素和 VCAM-1 表达,但不会使 PKC 易位。

DOI:
10.1006/bbrc.1993.1764
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发表时间:
1993
影响因子:
3.1
通讯作者:
Harlan,JM
Harlan,JM
中科院分区:
生物学4区
文献类型:
--
作者:
Deisher,TA;Sato,TT;Pohlman,TH;Harlan,JM

文献摘要

被引文献

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选择性βI同工酶蛋白激酶C(PKC)激动剂12-脱氧佛波醇13-苯乙酸酯20-乙酸酯(dPPA)诱导人脐静脉内皮细胞(HUVEC)NF-κ B样结合活性和E-选择素和VCAM-1的表面表达,类似于肿瘤坏死因子-α(TNF-α)的作用。PKC抑制剂Staurosporine和Ro 31 - 7549完全抑制dPPA对E-选择素和VCAM-1表达的诱导。PKC抑制剂也可降低TNF-α诱导的VCAM-1表达。然而,无论是dPPA还是TNF-α都没有将PKC从胞浆转移到HUVEC的质膜或核膜颗粒组分。这些结果表明,βI PKC同工酶的激活足以表达E-选择素和VCAM-1,并提示PKC可能介导TNF-α和dPPA的作用,而不需要通常与PKC激活相关的易位。
A protein kinase C (PKC) agonist selective for the βI isozyme, 12-deoxyphorbol 13-phenylacetate 20-acetate (dPPA), induced NF-κB-like binding activity and surface expression of E-selectin and VCAM-1 in human umbilical vein endothelial cells (HUVEC), similar to the effects of tumor necrosis factor-α (TNF-α). Induction of E-selectin and VCAM-1 expression by dPPA was completely inhibited by the PKC inhibitors staurosporine and Ro31 -7549. The PKC inhibitors also reduce TNF-α induced VCAM-1 expression. However, neither dPPA nor TNF-α translocated PKC from the cytosolic to the plasma or nuclear membrane particulate fractions in HUVEC. These results indicate that activation of the βI PKC isozyme is sufficient for expression of E-selectin and VCAM-1, and suggest that PKC may mediate the effects of TNF-α and dPPA without requiring the translocation normally associated with activation of PKC.