Modulation of Bcl-2 family proteins in primary endothelial cells during apoptosis
UNSPECIFIED (2002) Modulation of Bcl-2 family proteins in primary endothelial cells during apoptosis. PATHOPHYSIOLOGY OF HAEMOSTASIS AND THROMBOSIS, 32 (2). pp. 85-91. ISSN 1424-8832Full text not available from this repository.
We studied the expression of Bcl-2 family proteins during cytokine- and verotoxin (VT)-induced apoptosis in primary human umbilical vein endothelial cells (HUVECs). Our experiments demonstrated that high initial expression of Bcl-2 protein was significantly downregulated in HUVECs treated with IFN-gamma whereas TNF-alpha gave a less pronounced decrease in Bcl-2 level. Treatment with the combination of cytokines was more efficient in downregulating Bcl-2 protein. HUVECs pretreated with cytokines and incubated with VT gave a further significant decrease in Bcl-2 level. Simultaneous measurement of Bcl-xl level did not reveal any significant changes. Bax protein was upregulated in HUVECs stimulated with TNF-alpha alone or in combination with IFN-gamma. However, addition of VT did not give any further increase in Bax level suggesting that Bax upregulation is more important for cytokine- rather than VT-mediated apoptosis. Total endothelial cell growth factor deprivation gave a significant increase in apoptosis accompanied by a decrease of Bcl-2 in apoptotic cells while Bcl-xl and Bax levels were unaffected. Our data indicate that anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax are reciprocally regulated during apoptosis, whilst Bcl-xl is essentially unaffected. This implies that Bcl-2/Bax ratio rather than Bcl-xl controls apoptosis in primary endothelial cells. Copyright (C) 2002 S. Karger AG, Basel.
|Item Type:||Journal Article|
|Subjects:||R Medicine > RB Pathology|
|Journal or Publication Title:||PATHOPHYSIOLOGY OF HAEMOSTASIS AND THROMBOSIS|
|Number of Pages:||7|
|Page Range:||pp. 85-91|
Actions (login required)