ALTERED PHOSPHATIDYLINOSITOL BREAKDOWN AFTER K-ELASTIN STIMULATION IN PMNLS OF ELDERLY

被引：34

作者：

VARGA, Z ^{[1
]}

JACOB, MP ^{[1
]}

CSONGOR, J ^{[1
]}

ROBERT, L ^{[1
]}

LEOVEY, A ^{[1
]}

FULOP, T ^{[1
]}

机构：

[1] UNIV PARIS 12,FAC MED,BIOCHIM TISSU CONJONCT LAB,F-94010 CRETEIL,FRANCE

来源：

MECHANISMS OF AGEING AND DEVELOPMENT | 1990年 / 52卷 / 01期

关键词：

Elastin peptide; Inositol phosphates; Intracellular free Ca[!sup]2+[!/sup; Signal transduction mechanism;

D O I：

10.1016/0047-6374(90)90144-5

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The degradation of elastic fibres during atherosclerotic plaque formation in arterial wall is a well known process. The liberated elastin peptides such as K-elastin possess various biological activities: They are chemotactic for monocytes and fibroblasts, stimulate the oxidative burst and the intracellular free Ca2+ mobilisation through the phosphatidylinositol (PIP2) breakdown in PMNLs. It was found that the PIP2, breakdown induced by K-elastin is a pertussis toxin sensitive process in PMNLs of young subjects. In the case of the elderly, the K-elastin-induced oxidative burst, intracellular free Ca2+ elevation was less than in young, and could not be inhibited by pertussis toxin. Studying the K-elastin-induced inositol phosphate (IP) formation in PMNLs of elderly a disturbed PIP2 breakdown was found. K-elastin stimulated the IP formation at a very low level in PMNLs of elderly. This alteration of the second messenger formation (e.g. IP3 and Ca2+) after KE stimulation, might be the consequence of their originally elevated levels in resting PMNLs of elderly. © 1990.

引用

页码：61 / 70

页数：10

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