Inhibition of inflammatory endothelial responses by a pathway involving caspase activation and p65 cleavage.

Inhibition of inflammatory endothelial responses by a pathway involving caspase activation and p65 cleavage. Research Abstract Details 

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Inhibition of inflammatory endothelial responses by a pathway involving caspase activation and p65 cleavage. Abstract Text:

J Neuzil,A ,P von Hundelshausen,A Zernecke,T Weber,N Gellert,C Weber,

Suppression of NF kappa B activation has been involved in the elimination of survival programs during endothelial cell (EC) apoptosis. We used alpha-tocopheryl succinate (alpha-TOS) to trigger apoptosome formation and the subsequent activation of executioner caspases. The level of bcl-2 was reduced by alpha-TOS, and its downregulation potentiated and its overexpression suppressed pro-apoptotic effects of alpha-TOS, indicating a mitochondrial role in alpha-TOS-induced apoptosis in EC. alpha-TOS treatment was associated with induction of TUNEL-positive apoptosis in EC with a high but not with a low proliferation index. The use of the pan-caspase inhibitor z-VAD.fmk suggested the involvement of caspases in cleavage of p65, and in inhibition of nuclear translocation of p65 and NF kappa B-dependent transactivation of a gene construct encoding the green fluorescence protein elicited by TNF alpha in contact-arrested EC. The suppression by alpha-TOS of inflammatory EC responses induced by TNF alpha such as VCAM-1 mRNA and surface protein expression and shear-resistant arrest of monocytic cells were also reversed by z-VAD.fmk. NF kappa B-dependent transactivation was preserved in alpha-TOS-treated EC stably transfected with a caspase-noncleavable p65 mutant but not with its truncated form, thus establishing a direct link between alpha-TOS-induced effects and p65 cleavage. Our data infer a pathway by which caspase activation in EC inhibits NF kappa B-dependent inflammatory activation and monocyte recruitment, and provide evidence for a relationship between pro-apoptotic and anti-inflammatory pathways.

Inhibition of inflammatory endothelial responses by a pathway involving caspase activation and p65 cleavage. Publishing Authors By Initials

J Neuzil,A ,P von Hundelshausen,A Zernecke,T Weber,N Gellert,C Weber,

For similar heterocyclic compounds: heterocyclic compounds, 2-ring: benzopyrans: vitamin e research abstracts see: heterocyclic compounds: heterocyclic compounds, 2-ring: benzopyrans: vitamin e research

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Inhibition of inflammatory endothelial responses by a pathway involving caspase activation and p65 cleavage. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Biochemistry

VOLUME: 40

Page Numbers: 4686-92

Journal Abbreviation: Biochemistry

ISSN: 0006-2960

DAY: 17

MONTH: Apr

YEAR: 2001

Inhibition of inflammatory endothelial responses by a pathway involving caspase activation and p65 cleavage. Information

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LANGUAGE: eng

NlmUniqueID: 370623

Inhibition of inflammatory endothelial responses by a pathway involving caspase activation and p65 cleavage. Keywords Mesh Terms:

KEYWORDS: Vitamin E

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Inhibition of inflammatory endothelial responses by a pathway involving caspase activation and p65 cleavage. Information

Substance Name: Caspases

Registry Number: EC 3.4.22.-

Grant and Affiliation Information for Inhibition of inflammatory endothelial responses by a pathway involving caspase activation and p65 cleavage.

AFFILIATION: Institute for Prevention of Cardiovascular Diseases, Ludwig Maximilians University, Munich, Germany. jneuzil@klp.med.uni-muenchen.de

Country: United States

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MEDLINETA: Biochemistry

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