Apoptosis and Cell Death Channels in Prostate Cancer

Tapia-Vieyra, Juana Virginia; Mas‐Oliva, Jaime

doi:10.1016/s0188-4409(01)00274-0

Cited by 36 publications

(28 citation statements)

References 68 publications

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“…The PI molecule, a well-established cell death marker, enters necrotic or advanced-stage apoptotic cells, whereas YO-PRO-1 passes through cation channels in the plasma membrane, such as ATP-gated P2X7 receptor, which are activated in the early stage of cell apoptosis. 38,39 These small molecules are suitable for detecting endothelial cell apoptosis in vivo, because they can easily penetrate connective tissue and diffuse into microvessels. The results of microfluorography and TUNEL labeling show that under conditions after surgical exposure, microvascular endothelial cells in the SHR are committed to an apoptotic process more easily than in WKY rats, and higher cell apoptosis rate in the SHR is attenuated by antioxidants.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress Promotes Endothelial Cell Apoptosis and Loss of Microvessels in the Spontaneously Hypertensive Rats

Kobayashi

DeLano

Schmid‐Schönbein

2005

ATVB

116

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Objective-Endothelial cell apoptosis caused by oxidative stress may lead to the loss of microvessels (rarefaction) in hypertension. We examine here the effects of antioxidants on cell apoptosis and rarefaction. Methods and Results-The juvenile spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were treated with superoxide scavengers, Tempol or Tiron, during growth. After the treatment, oxidative stress status, endothelial cell apoptosis rate, and microvessel length density in skeletal muscle and mesentery were evaluated in comparison with age-matched controls. Untreated 16-week-old SHR had higher oxidative stress (PϽ0.01) and cell apoptosis rate (PϽ0.05) and lower microvessel length density (371Ϯ17 mm/mm 3 [PϽ0.01]) compared with age-matched WKY rats (435Ϯ15 mm/mm 3 ). In the SHR, but not in WKY rats, systemically applied antioxidants attenuated oxidative stress and cell apoptosis rate (PϽ0.05 versus untreated controls) and prevented the loss of microvessels (411Ϯ15 Key Words: arterial hypertension Ⅲ capillary Ⅲ endothelial cell apoptosis Ⅲ microvessels Ⅲ oxidative stress Ⅲ rarefaction Ⅲ superoxide A number of hypertensive animal models 1-3 and patients with essential hypertension 4 exhibit a reduction in microvessel length density in tissues such as skeletal muscle, skin, conjunctiva, and myocardium. This phenomenon, designated as structural or anatomic rarefaction, leads to an increase in peripheral vascular resistance and localized reduction in oxygen delivery to the tissue. 5 Substantial evidence indicates that microvascular rarefaction is associated with the pathogenesis of hypertension and may be accompanied by parenchymal cell death. 6,7 The disappearance of microvessels in hypertensive subjects may be a secondary event after blood pressure elevation. 8 However, recent research in man demonstrates microvascular rarefaction in pre-established stage of hypertensive subjects who still maintain near normal blood pressure. 9 In addition, the loss of microvessels is implicated in development of nonhypertensive pathologic conditions including diabetic organ failure. 10 These findings seem to suggest that factors other than elevated arterial pressure may promote the disappearance of microvessels. Accumulating evidence indicates that the increase in endothelial cell apoptosis in microvessels may cause rarefaction in hypertensive subjects, although the mechanism of enhanced cell apoptosis is still undergoing investigation. 11,12 We hypothesize that oxidative stress promotes endothelial cell apoptosis in microvessels and induces rarefaction in the spontaneously hypertensive rats (SHR). In the SHR, microvascular endothelium is exposed to enhanced oxidative stress due to an increase in xanthine-oxidase 13 and NADPH-oxidase activity 14 and/or a reduction in superoxide-dismutase activity. 15 Reactive oxygen species (ROS) modulate diverse functions and exert secondary effects on microvessels, eg, an inhibition of endothelium-dependent vasodilation 16 and a promotion of leukocyte adhesion to e...

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Section: Discussionmentioning

confidence: 99%

Oxidative Stress Promotes Endothelial Cell Apoptosis and Loss of Microvessels in the Spontaneously Hypertensive Rats

Kobayashi

DeLano

Schmid‐Schönbein

2005

ATVB

116

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“…Apoptosis and the cell cycle work together in maintaining cell homeostasis. Cancer cells will only be eliminated when the rate of cell death is greater than the rate of cell proliferation [29]. There are two main checkpoints in the control of cell cycle progression: G1/S preceding the replication process of DNA, and G2/M preceding the mitosis process.…”

Section: Discussionmentioning

confidence: 99%

Modulation of cell growth and apoptosis response in human prostate cancer cells supplemented with tocotrienols

Nesaretnam

Koon

Selvaduray

et al. 2008

Euro J Lipid Sci & Tech

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Previous studies have shown that tocotrienols are powerful growth inhibitors and potent inducers of apoptosis in human breast cancer cells. The objective of the current study was to examine effects of tocotrienols on apoptotic signals in androgen-independent PC-3 human prostate cancer cells. We investigated the effects of the tocotrienol-rich fraction (TRF) from palm oil, a-tocopherol (aT), a-tocotrienol (aT 3 ), g-tocotrienol (gT 3 ) and d-tocotrienol (dT 3 ) on PC-3 cell growth. TRF inhibited PC-3 growth with a nonlinear response, with complete growth suppression at 10 mg/mL. dT 3 and gT 3 showed complete cell inhibition at 8 mg/mL whilst aT had no effect. dT 3 and gT 3 showed the most promise in the cell growth assays, and all subsequent experiments were performed with dT 3 , TRF and aT. TRF and dT 3 at 8 mg/mL induced apoptosis in PC-3 cells after 48 h of treatment. In addition, TRF and dT 3 treatments were able to affect the cell cycle, with accumulation in the S phase, G2 phase block and increases in SubG1 by 72 h. We then proceeded to investigate the expression levels of Fas receptor and Fas ligand, caspase 8, caspase 3 and bax in PC-3 cells following treatment with tocotrienols using real-time PCR and Western blot methods. TRF and dT 3 at 8 mg/mL increased Fas ligand expression levels by 368 and 456%, respectively, after 24 h and Fas receptor expression levels by 210% and 356%, respectively, after 48 h. TRF-and dT 3 -treated PC-3 cells overexpressed caspase 8 and bax protein after 24 h, and caspase 3 after 48 h. In conclusion, tocotrienols are able to induce apoptosis and cell cycle arrest in PC-3 cells, with increased expression of Fas receptor, Fas ligand, caspase 8, caspase 3 and bax, suggesting a potential role in chemoprevention of prostate cancer.

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“…Cell death as well as cell proliferation and differentiation are important for homeostasis. Cells undergoing PCD are characterized by morphological changes, including cellular shrinkage, plasma and nuclear membrane blebbing, organelle relocalization and compaction, nuclear DNA condensation with or without fragmentation, and hypersegmentation of nuclear chromatin of irregular size [28][29][30] . These hypersegmented nuclear structures may then bud from the rapidly blebbing cell surface to form "apoptotic bodies" 31 .…”

Section: Effects On Programmed Cell Deathmentioning

confidence: 99%