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
中科院分区:
文献类型:
--
作者:
Deisher,TA;Sato,TT;Pohlman,TH;Harlan,JM
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.