Molecular and morphological modifications occurring in rat heart exposed to intermittent hypoxia: role for protein kinase C α

Cataldi, Amelia; Bianchi, G.; Rapino, Cinzia; Sabatini, Nadia; Centurione, Lucia; Giulio, Camillo Di; Bosco, Domenico; Antonucci, Adriano Torres

doi:10.1016/j.exger.2003.11.010

Cited by 23 publications

(31 citation statements)

References 31 publications

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“…Schumacker and coworkers have shown that cardiac myocytes do sense low oxygen tension via activating the production of ROS from mitochondria [88][89][90]. Cataldi et al [91] reported that protein kinase C alpha is involved in sensing intermittent hypoxia in the rat heart. Wright et al [92] showed that prolyl hydroxylation is the oxygen-sensing mechanism in cardiac myocytes, which in turn regulates HIF-1, heme oxygenase-1, and GLUT1.…”

Section: Oxidative Stress In Animal Models Of Intermittent Hypoxiamentioning

confidence: 99%

Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases

Suzuki

Jain

Park

et al. 2006

Free Radical Biology and Medicine

205

123

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Obstructive sleep apnea (OSA) has emerged as a major public health problem and increasing evidence indicates that untreated OSA can lead to the development of various cardiovascular disorders. One important mechanism by which OSA may promote cardiovascular diseases is intermittent hypoxia, in which patients are subjected to repeated episodes of brief oxygen desaturation in the blood, followed by reoxygenation. Such cycles of hypoxia/reoxygenation may result in the generation of reactive oxygen species. Some studies have demonstrated the presence of oxidative stress in OSA patients as well as in animals subjected to intermittent hypoxia. Further, modulations of nitric oxide and biothiol status might also play important roles in the pathogenesis of OSA-associated diseases. Reactive oxygen species and redox events are also involved in the regulation of signal transduction for oxygen-sensing mechanisms. This review summarizes currently available information on the evidence for and against the occurrence of oxidative stress in OSA and the role of reactive oxygen species in cardiovascular changes associated with OSA.

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Section: Oxidative Stress In Animal Models Of Intermittent Hypoxiamentioning

confidence: 99%

Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases

Suzuki

Jain

Park

et al. 2006

Free Radical Biology and Medicine

205

123

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“…Formaldehyde-fixed cerebral cortices were embedded in paraffin and left frontal sections stained with haematoxylin-eosin (Cataldi et al, 2004). Neuronal cell density was determined by direct visual counting of ten fields for each of five slides per sample at 40× magnification.…”

Section: Light Microscopy and Immunohistochemistrymentioning

confidence: 99%

“…In addition, intermittent hypoxia (e.g. 12% O 2 for 12 h followed by reoxygenation for 12 h) is a more potent inducer of cell death than continuous hypoxia, probably as a result of a substantial increase in reactive oxygen species (ROS) generation (Cataldi et al ., 2004). Increased ROS levels may lead to cell death, accelerated aging and the appearance of age-related diseases (Finkel & Holbrock, 2000;Wickens, 2001).…”

Section: Introductionmentioning

confidence: 99%

HIF‐1α cytoplasmic accumulation is associated with cell death in old rat cerebral cortex exposed to intermittent hypoxia

Rapino¹,

Bianchi²,

Giulio³

et al. 2005

Aging Cell

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SummaryIntermittent hypoxia, followed by reoxygenation, determines the production of reactive oxygen species (ROS), which may lead to accelerated aging and to the appearance of age-related diseases. The rise in ROS levels might constitute a stress-stimulus activating specific redoxsensitive signalling pathways, so inducing either damaging or protective functions. Here, we report that in old rat cerebral cortex exposed to hypoxia, the accumulation in the cytoplasm of hypoxic inducible factor 1α α α α (HIF-1α α α α ) -the master regulator of oxygen homeostasis -concomitant with p66Shc activation and reduced IkBα α α α phosphorylation is associated with tissue apoptosis or necrosis. In young cerebral cortex, we hypothesize that the hypoxic damage may be reversible, based on our demonstration of elevated HIF-1α α α α levels, combined with a low level of IkBα α α α phosphorylation, a decrease in IAP-1 and a lack of major change in Bcl2 family proteins. These observations are associated with a low level of cell death induced by hypoxia, suggesting that HIF-1α α α α activation in cortical neurons may produce rescue proteins in response to intermittent hypoxia.

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“…As an example to a positive result, it has been shown that short cycled, mild intermittent hypoxia induced HIF-1α pathway in rabbit heart (15). However, in another study, although intermittent hypoxia induced the nuclear translocation of HIF-1α protein with following increase in VEGF protein, the myocardial expression of HIF-1α protein was not found to be increased (8). This result was similar to our finding showing that the increase of VEGF mRNA expression was not associated with an increase in HIF-1α mRNA expression in the left ventricle.…”

Section: Discussionmentioning

confidence: 90%

“…There was limited number of studies related to the heart tissue. Furthermore, the hypoxia protocols used in these studies were different (7)(8)(9). It has been shown in an immunohistochemical study that, the exposure of intermittent hypoxia 12h/ day, for 12 days, did not increase the expression of HIF-1α protein in the rat heart (8).…”

Section: Introductionmentioning

confidence: 99%

The effects of acute and intermittent hypoxia on the expressions of HIF-1α and VEGF in the left and right ventricles of the rabbit heart

Tekin¹,

Dursun²,

Baştuğ³

et al. 2011

Anadolu Kardiyol Derg

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Molecular and morphological modifications occurring in rat heart exposed to intermittent hypoxia: role for protein kinase C α

Cited by 23 publications

References 31 publications

Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases

Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases

HIF‐1α cytoplasmic accumulation is associated with cell death in old rat cerebral cortex exposed to intermittent hypoxia

The effects of acute and intermittent hypoxia on the expressions of HIF-1α and VEGF in the left and right ventricles of the rabbit heart

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