Proliferative Response of Smooth Muscle Cells in Hypertension

Printseva, O. Yu.; Tjurmin, A. V.

doi:10.1093/ajh/5.6.118s

Cited by 14 publications

(8 citation statements)

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“…25 For example, markers of endothelial dysfunction have been used to derive prognostic clinical information 6 and monitor therapy. In addition, increases in arterial blood pressure induce proliferation of vascular smooth muscle cells 26 and change their phenotype 27 and sensitivity to and conductance of calcium. 28 These observations denote the wide array of deleterious changes that HT provokes in the vascular wall.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Antioxidant Intervention Improves Myocardial Microvascular Function in Experimental Hypertension

et al. 2004

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Abstract-Hypertension increases oxidative stress, which can impair myocardial microvascular function and integrity.However, it is yet unclear whether long-term antioxidant intervention in early hypertension would preserve myocardial perfusion and vascular permeability responses to challenge. Pigs were studied after 12 weeks of renovascular hypertension without (nϭ8) or with daily supplementation of antioxidants (100 IU/kg vitamin E and 1 g vitamin C, nϭ6), and compared with normal controls (nϭ7). Myocardial perfusion and microvascular permeability were measured in vivo by electron beam computed tomography before and after 2 cardiac challenges (intravenous adenosine and dobutamine). Basal left ventricular muscle mass was also obtained. 4,5 In addition to its effect on vascular reactivity, HT has effects on other functions of the vascular wall. Increases in blood pressure can also lead to alterations in thrombogenesis 6 and increased permeability of the endothelium. 7,8 One of the mechanisms that might be responsible for HT-induced myocardial dysfunction is an increase in oxidative stress, which has been demonstrated in both humans 9 and animal models. 10 Indeed, short-term antioxidant administration improved coronary epicardial endothelial function. 9,11 However, whether long-term antioxidant supplementation might preserve HT-induced myocardial microvascular dysfunction remains unclear.Electron beam computed tomography (EBCT), a fast CT scanner, provides a unique tool to accurately 12 and reproducibly 13 study in vivo transmural myocardial perfusion 14 -16 and myocardial microvascular permeability (MVP) 15-17 noninvasively. This tool provides an opportunity to explore noninvasively the effect of long-term therapeutic interventions on myocardial vascular function. Thus, the present study was designed to test the hypothesis that long-term antioxidant blockade would preserve myocardial vascular function in early HT. Methods AnimalsAll of the study procedures were approved by the Institutional Animal Care and Use Committee. Twenty-one female, domestic crossbred pigs (Pork Partners, Stewartville, Minn; 55 to 65 kg each) were studied after a 12-week preparation: one group (normal, nϭ7) was untreated, and in the second (HT, nϭ8), renovascular HT was induced by placing a local-irritant stent in the left renal artery, as previously described. 16,18 In addition to induction of renal artery stenosis, animals from group 3 (HTϩantioxidants [Ao], nϭ6) received daily oral antioxidant supplementation (combination of 100 IU/kg vitamin E and 1 g vitamin C). This dosage was based on our previous studies in pigs that showed that this combination provided

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Section: Discussionmentioning

confidence: 99%

Long-Term Antioxidant Intervention Improves Myocardial Microvascular Function in Experimental Hypertension

et al. 2004

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“…This context demonstrates the importance of tight regulation, not only of ploidy but also the degree of polyploidy. Hypertensive individuals display a significant increase in VSMC ploidy and hypertrophy 74, which leads to arterial stiffness, left ventricular overload and altered coronary blood perfusion 75. Angiotensin II, which promotes vascular constriction and hypertension, can mediate cell polyploidization through the Akt1 signalling pathway.…”

Section: Cytokinesis Failurementioning

confidence: 99%

Cytokinesis, ploidy and aneuploidy

Lacroix

Maddox

2011

The Journal of Pathology

120

102

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Cytokinesis is the last step of cell division that physically separates the daughter cells. As such, it ensures the proper inheritance of both nuclear and cytoplasmic contents. Accomplishment of cytokinesis in eukaryotes is dictated by several key events: establishment of the division plane, furrow ingression through contraction of an actomyosin ring and abscission via membrane fusion. Most mammalian somatic cells are diploid. Polyploidy can result from cytokinesis failure and may contribute to the development of pathologies such as cancer. However, polyploidy is essential for cellular differentiation and function in some contexts (eg hepatocytes, megakaryocytes and others). Consequently, the degree of ploidy and the achievement of cytokinesis must be tightly regulated throughout an organism and among different cell types. In this review we will highlight several examples of normal and pathological polyploidy, focusing on those caused by a controlled failure or dysregulation of cytokinesis, respectively. Last, we propose therapeutic routes to control cytokinesis to restore or block cell division.

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“…Other alterations of the cell cycle control such as VSMC polyploidization are frequently seen associated with agerelated hypertension [12,13]. The aim of the present study was to examine alterations in VSMC's CKI expression because of aging www.bioscirep.org / Volume 30 (1) / Pages [11][12][13][14][15][16][17][18] in both cell culture and arterial tissues. Our results demonstrate that aging produces an up-regulation of p16 INK4a expression in VSMCs, which may be a worsening factor in the development of age-related vascular diseases.…”

Section: Introductionmentioning

confidence: 99%

Aging increases p16INK4a expression in vascular smooth-muscle cells

et al. 2009

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Alteration of VSMC (vascular smooth-muscle cell) physiology is associated with the development of atherosclerosis and restenosis. We hypothesize that aging up-regulates the expression of p16 INK4a in VSMCs, which may increase the susceptibility of blood vessels to vascular occlusive diseases. Aortic VSMCs were obtained from young and aged mice. Cells from aged mice grew more slowly than those from their younger counterparts. Progression of cell cycle in response to serum stimulation was significantly inhibited in those cells with aging, as determined by FACS after propidium iodide staining. A significant up-regulation of p16 INK4a (2.5-fold, P=0.0012) was found in VSMC from aged animals using gene arrays. The up-regulation of this gene was further confirmed by quantitative RT-PCR (reverse transcription-PCR) and Western-blot experiments. Immunostaining for p16 INK4a confirmed that aortas from aged mice contained more p16 INK4a+ SMA (smooth-muscle cell actin)+ cells than aortas from young animals (26.79+/-2.45 versus 7.06+/-1.44, P=0.00027, n=4). In conclusion, we have shown that aging up-regulates the expression of p16 INK4a in VSMC in both cultures and arteries. The increase in p16 INK4a in the vasculature with aging may modify VSMC's response to post-injury stress and therefore accelerate the development of age-related cardiovascular diseases.

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Proliferative Response of Smooth Muscle Cells in Hypertension

Cited by 14 publications

References 0 publications

Long-Term Antioxidant Intervention Improves Myocardial Microvascular Function in Experimental Hypertension

Long-Term Antioxidant Intervention Improves Myocardial Microvascular Function in Experimental Hypertension

Cytokinesis, ploidy and aneuploidy

Aging increases p16INK4a expression in vascular smooth-muscle cells

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