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Modulation of intercellular communication between smooth muscle cells by growth factors and cytokines.

Abstract：

:We recently reported that tumor necrosis factor alpha is able to cause a dose-dependent and persistent reduction in gap junctional intercellular communication between primary human smooth muscle cells. In order to study whether this observed persistent reduction in gap junctional intercellular communication is a unique feature for tumor necrosis factor alpha, the present study focuses on the effects of other growth factors and cytokines on gap junctional intercellular communication. Platelet-derived growth factor AA and BB (PDGF-AA, PDGF-BB), basic fibroblast growth factor (bFGF), interleukin-6 and interferon-gamma were able to modulate gap junctional intercellular communication between primary human smooth muscle cells in vitro. However, our results demonstrate that the magnitude and nature of the observed effects are growth factor- and cytokine-specific. PDGF-AA, PDGF-BB and interleukin-6 caused a transient reduction in gap junctional intercellular communication, while bFGF induced a transient increase in gap junctional intercellular communication. Interferon-gamma was shown to be capable of causing a persistent reduction in gap junctional intercellular communication. In addition, PDGF-AA, PDGF-BB, bFGF, interleukin-6, interferon-gamma and tumor necrosis factor alpha all stimulated smooth muscle cell proliferation. These observations suggest a more complex relationship between modulation of gap junctional intercellular communication and cell proliferation than current hypotheses imply. The implications of the observed effects of growth factors and cytokines on gap junctional intercellular communication between smooth muscle cells in relation to the process of atherosclerosis is discussed.

journal_name

Eur J Pharmacol

journal_title

European journal of pharmacology

authors

Mensink A,Brouwer A,Van den Burg EH,Geurts S,Jongen WM,Lakemond CM,Meijerman I,Van der Wijk T

doi

10.1016/0014-2999(96)00368-8

subject

Has Abstract

pub_date

1996-08-22 00:00:00

pages

73-81

issue

1

eissn

0014-2999

issn

1879-0712

pii

0014-2999(96)00368-8

journal_volume

310

pub_type

杂志文章

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