Altered phosphatidylinositol breakdown after K-elastin stimulation in PMNLs of elderly

Zsuzsa Varga, Marie Paule Jacob, József Csongor, Ladislas Robert, András Leövey, Tamaás Fülöp

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)61-70
Number of pages10
JournalMechanisms of Ageing and Development
Volume52
Issue number1
DOIs
Publication statusPublished - Mar 1 1990

Fingerprint

Elastin
Phosphatidylinositols
Inositol Phosphates
Respiratory Burst
Pertussis Toxin
Elastic Tissue
Second Messenger Systems
Atherosclerotic Plaques
Fibroblasts
Bioactivity
Monocytes
Degradation
Peptides
Fibers

Keywords

  • Elastin peptide
  • Inositol phosphates
  • Intracellular free Ca
  • Signal transduction mechanism

ASJC Scopus subject areas

  • Ageing
  • Biochemistry
  • Developmental Biology
  • Developmental Neuroscience

Cite this

Altered phosphatidylinositol breakdown after K-elastin stimulation in PMNLs of elderly. / Varga, Zsuzsa; Jacob, Marie Paule; Csongor, József; Robert, Ladislas; Leövey, András; Fülöp, Tamaás.

In: Mechanisms of Ageing and Development, Vol. 52, No. 1, 01.03.1990, p. 61-70.

Research output: Contribution to journalArticle

Varga, Zsuzsa ; Jacob, Marie Paule ; Csongor, József ; Robert, Ladislas ; Leövey, András ; Fülöp, Tamaás. / Altered phosphatidylinositol breakdown after K-elastin stimulation in PMNLs of elderly. In: Mechanisms of Ageing and Development. 1990 ; Vol. 52, No. 1. pp. 61-70.
@article{452e58a04ee14965a79bdad52cf8fd3b,
title = "Altered phosphatidylinositol breakdown after K-elastin stimulation in PMNLs of elderly",
abstract = "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.",
keywords = "Elastin peptide, Inositol phosphates, Intracellular free Ca, Signal transduction mechanism",
author = "Zsuzsa Varga and Jacob, {Marie Paule} and J{\'o}zsef Csongor and Ladislas Robert and Andr{\'a}s Le{\"o}vey and Tama{\'a}s F{\"u}l{\"o}p",
year = "1990",
month = "3",
day = "1",
doi = "10.1016/0047-6374(90)90144-5",
language = "English",
volume = "52",
pages = "61--70",
journal = "Mechanisms of Ageing and Development",
issn = "0047-6374",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

TY - JOUR

T1 - Altered phosphatidylinositol breakdown after K-elastin stimulation in PMNLs of elderly

AU - Varga, Zsuzsa

AU - Jacob, Marie Paule

AU - Csongor, József

AU - Robert, Ladislas

AU - Leövey, András

AU - Fülöp, Tamaás

PY - 1990/3/1

Y1 - 1990/3/1

N2 - 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.

AB - 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.

KW - Elastin peptide

KW - Inositol phosphates

KW - Intracellular free Ca

KW - Signal transduction mechanism

UR - http://www.scopus.com/inward/record.url?scp=0025037821&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025037821&partnerID=8YFLogxK

U2 - 10.1016/0047-6374(90)90144-5

DO - 10.1016/0047-6374(90)90144-5

M3 - Article

C2 - 2156116

AN - SCOPUS:0025037821

VL - 52

SP - 61

EP - 70

JO - Mechanisms of Ageing and Development

JF - Mechanisms of Ageing and Development

SN - 0047-6374

IS - 1

ER -