DNA damage, p53, apoptosis and vascular disease

Angiotensin II (Ang II), which plays a pivotal role in the pathophysiology of the two-kidney, one-clip (2K1C) Goldblatt hypertension, has been associated with augmented generation of reactive oxygen species (ROS) in some cells and tissues. In the present study, we evaluated the influence of 2K1C hypertension on oxidative stress, DNA fragmentation, and apoptosis of bone marrow (BM) cells. Two weeks after the renal artery clipping or Sham operation, flow cytometry analysis showed a higher production of superoxide anions (approximately sixfold) and hydrogen peroxide (approximately twofold) in 2K1C hypertensive than in Sham normotensive mice. 2K1C mice also showed an augmented DNA fragmentation (54%) and apoptotic cells (21%). Our data show that the 2K1C renovascular hypertension is characterized by an increased production of ROS, DNA damage, and apoptosis of BM, which is a fundamental source of the cells involved in tissue repair.

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“…compromising the energy supply and consequently apoptosis (Polyak et al, 1997;Mercer et al, 2007;Yu et al, 2012).…”

Section: K1c Hypertension Affects Bone Marrow Cellsmentioning

confidence: 99%

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

Campagnaro

Tonini

Doche

et al. 2013

DNA and Cell Biology

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“…20 But, none of these studies identified the lineage of the proliferating/dying cells, and none of these studies examined the specific role of p53 knockout in VSMCs. 21 So the proatherogenic effects of p53 deficiency cannot yet be definitively explained by either an increase in cellular proliferation or a decrease in apoptosis. 22 And, whether p53 activation provokes apoptosis or growth arrest, either reversible or permanent, depends on the context and cellular type.…”

Section: Discussionmentioning

confidence: 99%

“…Some studies have shown that p53 can induce the expression of some inflammation factors, which in turn can induce carotid atherosclerosis, through endothelial dysfunction. 35 Additionally, unwanted byproducts of an inappropriate cellular environment (eg, hypercholesterolemia) can also lead to an increase in carotid atherosclerosis, one mechanism of which could be the up-regulation of ICAM-1. 36 One study has also shown that p53 activation in senescent cells is responsiblefor an enhanced expression of CAMs, which can play a role in certain age-related aberrations.…”

Section: Discussionmentioning

confidence: 99%

p53 Levels Positively Correlate with Carotid Intima‐media Thickness in Patients with Subclinical Atherosclerosis

Chen

Wang

et al. 2009

Clinical Cardiology

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Background: The level of circulating p53 is related to inflammation in asymptomatic subjects with cardiovascular risk factors. Whether p53 is associated with the severity of atherosclerosis remains to be determined. Hypothesis: This study examines the relationship of systemic p53 levels with atherosclerotic risk factors and subclinical atherosclerosis. Methods: Circulating levels of p53 and markers of inflammation were measured in 356 subjects with cardiovascular risk factors but who were free from clinical cardiovascular disease. Subclinical atherosclerosis was evaluated by both the mean carotid intima-media thickness (IMT) and the presence of atherosclerotic plaques with the use of B-mode ultrasound in all subjects. Results: p53 levels were positively correlated with age (r = 0.382, P < 0.001), intercellular adhesion molecular-1 (ICAM-1; r = 0.510, P < 0.01), vascular cell adhesion molecular-1 (VCAM-1; r = 0.497, P < 0.01), E-selectin (r = 0.337, P < 0.01), and carotid IMT (r = 0.594, P < 0.01). The association between p53 and IMT remained significant in multiple regression analysis (P < 0.01) when controlling for traditional atherosclerotic risk factors and inflammatory markers. Conclusion: Higher plasma p53 levels were associated with an increase in inflammatory markers, as well as increased carotid IMT. Circulating p53 may be useful in identifying subclinical atherosclerosis in subjects symptomatically free from cardiovascular disease.

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“…Furthermore, SAA has been shown to induce the expression of the pro-inflammatory cytokine, IL-8, as mediated via IκB degradation and NF-κB activation 21) . Apoptosis is also known to be a key event in atherosclerosis, with the observation of a correlation between the frequency of apoptosis and stage of atherosclerotic lesions [22][23][24][25] . Due to poor efferocytosis, apoptosis of vascular cells within atherosclerotic plaques can affect the stability and structure of these lesions, resulting in the formation of unstable plaques 26) .…”

Section: Quantitative Real-time Pcrmentioning

confidence: 99%

The Atherogenic Effects of Serum Amyloid A are Potentially Mediated via Inflammation and Apoptosis

Tan

Ooi

Shen

et al. 2014

JAT

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DNA damage, p53, apoptosis and vascular disease

Cited by 94 publications

References 86 publications

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

p53 Levels Positively Correlate with Carotid Intima‐media Thickness in Patients with Subclinical Atherosclerosis

The Atherogenic Effects of Serum Amyloid A are Potentially Mediated via Inflammation and Apoptosis

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