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Interference with c-myc expression and RB phosphorylation during TNF-mediated growth arrest in human endothelial cells.

Abstract：

:Incorporation of [3H]-thymidine into DNA in non-synchronized cultures of human endothelial cells was blocked by a 24 h exposure to TNF in a dose dependent manner that resulted in accumulation of cells in G1, as assayed by flow cytometry analysis of DNA content. Proliferation restarted when cells were replated in the absence of TNF. Northern analysis of c-myc mRNA in synchronized untreated cultures showed a transient increase previous to DNA synthesis that was decreased with TNF treatment. Western analysis of the retinoblastoma gene product RB in untreated synchronized cultures showed reduced electrophoretic mobility during the transition from G1 to S, congruent with RB inactivation by phosphorylation. TNF treatment prevented RB retardation and reduced total levels of RB protein. Taken together our results show that the TNF-mediated block of endothelial proliferation correlates with deficient activation of the G1 events necessary for entry into S, despite the presence of serum and endothelial mitogens.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

López-Marure R,Bernal AE,Zentella A

doi

10.1006/bbrc.1997.7056

subject

Has Abstract

pub_date

1997-07-30 00:00:00

pages

819-24

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(97)97056-X

journal_volume

236

pub_type

杂志文章

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