Hypoxia-induced apoptosis in endothelial cells and embryonic stem cells

Lee, Chien‐Nan; Cheng, Wen-Fang; Chang, Ming; Su, Yi‐Ning; Chen, C A; Hsieh, Fon Jou

doi:10.1007/s10495-005-2946-0

Cited by 37 publications

(25 citation statements)

References 26 publications

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“…Under hypoxic conditions survival and proliferation of the cells were impaired, while in a normoxic atmosphere cell damage was even more severe. For glucose/serum starved HUVECs, hypoxia apparently acts as protective factor, while other groups described deleterious effects of hypoxia on HUVECs and mature endothelial cells kept in normal medium [15,16,17]. The damage to glucose/serum starved HUVECs was alleviated by CBMSC-conditioned medium, which reduced apoptotic and necrotic cell death and increased the number of metabolically active cells with preserved proliferative capacity.…”

Section: Discussionmentioning

confidence: 99%

Cord Blood Mesenchymal Stromal Cell-Conditioned Medium Protects Endothelial Cells via STAT3 Signaling

Bader

Brodarac

Klose

et al. 2014

Cell Physiol Biochem

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Background/Aims: Cell-based therapies may be useful for treating ischemic diseases, but the underlying mechanisms are incompletely understood. We investigated the impact of cord blood mesenchymal stromal cell (CBMSC)- or fibroblast (FB)-secreted factors on starved endothelial cells and determined the relevant intracellular signaling pathways. Methods: HUVECs were subjected to glucose/serum deprivation (GSD) in hypoxia or normoxia, in presence of CBMSC- or FB-conditioned medium (CM). Viability and proliferation were determined via WST-8 conversion and BrdU incorporation. Apoptosis was quantified by annexin V/ethidium homodimer-III staining, nuclear fragmentation and cell morphology. mRNA expression and protein phosphorylation were determined by real-time qPCR and western blot. Experiments were repeated in presence of small-molecule inhibitors. Results: The negative impact of GSD was most pronounced at 21% O₂. Here, medium of CBMSCs and FBs increased viability and proliferation and reduced apoptosis of HUVECs. This was associated with increased STAT3 and ERK1/2 phosphorylation and BCL-2 expression. Under STAT3 inhibition, the beneficial effect of CBMSC-CM on viability and BCL-2 expression was abolished. Conclusion: Factors released by CBMSCs protect endothelial cells from the deleterious impact of GSD by activation of the STAT3 survival pathway. However, this phenomenon is not CBMSC-specific and can be reproduced using juvenile fibroblasts.

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Section: Discussionmentioning

confidence: 99%

Cord Blood Mesenchymal Stromal Cell-Conditioned Medium Protects Endothelial Cells via STAT3 Signaling

Bader

Brodarac

Klose

et al. 2014

Cell Physiol Biochem

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“…Unfortunately, the predilection site of eroded plaques in humans has not been well elucidated until now. It has been also reported that hypoxia, oxLDL, homocysteine, oxygen-derived free radicals and some cytokines in blood can induce endothelial cell apoptosis (Isner et al 1995;Konno et al 1999;Mercie et al 2000;Lee et al 2005). Some researchers also demonstrated that apoptosis-induced genes like Bax, Fas and p53 were upregulated in atherosclerotic plaques (Kockx 1998).…”

Section: Discussionmentioning

confidence: 99%

Endothelial Cell Apoptosis is Responsible for the Formation of Coronary Thrombotic Atherosclerotic Plaques

Sun

Chen

et al. 2009

Tohoku J. Exp. Med.

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“…The p53 tumor suppressor is a ubiquitously-expressed transcription factor that is activated by DNA damage (D'Sa-Eipper et al, 2001;Katayama et al, 2002) and other cellular stressors, such as hypoxia (Long et al, 1997;Lee et al, 2005). The primary function of this protein is to induce cells to undergo G 1 arrest (Xiong et al, 1993;elDeiry et al, 1994) or apoptosis by activating the appropriate target genes.…”

Section: Genetic Models Of Cell Death In Mouse Placentamentioning

confidence: 99%

Molecular mechanisms of trophoblast survival: From implantation to birth

2005

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Fetal development depends upon a coordinated series of events in both the embryo and in the supporting placenta. The initial event in placentation is appropriate lineage allocation of stem cells followed by the formation of a spheroidal trophoblastic shell surrounding the embryo, facilitating implantation into the uterine stroma and exclusion of oxygenated maternal blood. In mammals, cellular proliferation, differentiation, and death accompany early placental development. Programmed cell death is a critical driving force behind organ sculpturing and eliminating abnormal, misplaced, nonfunctional, or harmful cells in the embryo proper, although very little is known about its physiological function during placental development. This review summarizes current knowledge of the cell death patterns and molecular pathways governing the survival of cells within the blastocyst, with a focus on the trophoblast lineage prior to and after implantation. Particular emphasis is given to human placental development in the context of normal and pathological conditions. As molecular pathways in humans are poorly elucidated, we have also included an overview of pertinent genetic animal models displaying defects in trophoblast survival.

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Hypoxia-induced apoptosis in endothelial cells and embryonic stem cells

Abstract: Hypoxia increases both HUVEC and mouse EB apoptosis, which is associated with increase in p53/Bax expression.

Cited by 37 publications

References 26 publications

Cord Blood Mesenchymal Stromal Cell-Conditioned Medium Protects Endothelial Cells via STAT3 Signaling

Cord Blood Mesenchymal Stromal Cell-Conditioned Medium Protects Endothelial Cells via STAT3 Signaling

Endothelial Cell Apoptosis is Responsible for the Formation of Coronary Thrombotic Atherosclerotic Plaques

Molecular mechanisms of trophoblast survival: From implantation to birth

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