Mechanical strain-induced human vascular matrix synthesis: The role of angiotensin II

Stanley, Adrian G.; Patel, H.; Knight, A.L.; Williams, Bryan

doi:10.3317/jraas.2000.007

Cited by 42 publications

(27 citation statements)

References 19 publications

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“…27 Numerous studies have demonstrated that angiotensin II through AT1 receptor induces VSM cell proliferation and hypertrophy and has an essential role in extracellular matrix expansion. [29][30][31][32] Furthermore, Candesartan and cavernous tissue in SHR JE Toblli et al cell culture, animal models and clinical studies have supported the idea that AT1 receptor activation causes vascular superoxide release in vitro and in vivo leading to impairment of endothelium-dependent vasodilation. 33,34 In agreement with these findings, inhibition of AT1 receptor activation by AT1 receptor antagonist or ACE inhibitors improves endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 96%

Candesartan cilexetil protects cavernous tissue in spontaneously hypertensive rats

Toblli

Stella²,

Mazza

et al. 2004

Int J Impot Res

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In previous experiments, our group demonstrated morphological changes in erectile tissue from male spontaneously hypertensive rats (SHR). The present study was performed to determine whether an angiotensin II receptor blocker could protect cavernous tissue (CT) from these structural alterations in SHR. Male SHR and Wistar-Kyoto (WKY) rats were studied during 4 months. Rats were divided into three groups: SHR (n ¼ 10), SHR with candesartan cilexetil (n ¼ 10) and WKY rats (n ¼ 10). Candesartan cilexetil 7.5 mg/kg/day was administered orally throughout the study. CT was processed for pathology studies. The amount of (1) cavernous smooth muscle (CSM), (2) vascular smooth muscle (VSM), (3) collagen type III, and the rat endothelial cell antibody (RECA-1)/tunica media ratio in cavernous arteries were evaluated. SHR with candesartan cilexetil showed a lower blood pressure, a lower percentage of CSM, smaller VSM area, with a higher RECA-1/media ratio, and a lower percentage of collagen type III, when compared to untreated SHR. In addition, SHR showed a positive correlation between systolic blood pressure (SBP) and CSM amount (r ¼ 0.91; Po0.01), and SBP and the percentage of collagen type III (r ¼ 0.88; Po0.01); these correlations were not observed either in SHR treated with candesartan cilexetil or in WKY rats. We conclude that candesartan cilexetil provides a significant protective role against morphologic changes in vessels as well as in cavernous spaces of the erectile tissue, caused by high blood pressure, in SHR.

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Section: Discussionmentioning

confidence: 96%

Candesartan cilexetil protects cavernous tissue in spontaneously hypertensive rats

Toblli

Stella²,

Mazza

et al. 2004

Int J Impot Res

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“…In experimental models of hypertension, including suprarenal abdominal aorta constriction, ANG II acting directly and/or indirectly via the synthesis of peptide growth factors EGF and TGF-␤ significantly influenced vascular and cardiac remodeling (10,22,29,30,33,35,40). On the basis of these observations, we performed in vitro experiments to assess the impact of ANG II, EGF, and TGF-␤ 1 on nestin expression in cultured vascular smooth muscle cells.…”

Section: Discussionmentioning

confidence: 99%

Nestin upregulation characterizes vascular remodeling secondary to hypertension in the rat

Tardif

Hertig

Duquette

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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The present study tested the hypothesis that vessel remodeling secondary to hypertension was characterized by nestin upregulation in vascular smooth muscle cells. Two weeks after suprarenal abdominal aorta constriction of adult male Sprague-Dawley rats, elevated mean arterial pressure increased the media area and thickness of the carotid artery and aorta and concomitantly upregulated nestin protein levels. In the normal adult rat carotid artery, nestin immunoreactivity was observed in a subpopulation of vascular smooth muscle cells, and the density significantly increased following suprarenal abdominal aorta constriction. Filamentous nestin was detected in cultured rat carotid arteryand aorta-derived vascular smooth muscle cells and an analogous paradigm observed in human aorta-derived vascular smooth muscle cells. ANG II and EGF treatment of vascular smooth muscle cells stimulated DNA and protein synthesis and increased nestin protein levels. Lentiviral short-hairpin RNA-mediated nestin depletion of carotid artery-derived vascular smooth muscle cells inhibited peptide growth factor-stimulated DNA synthesis, whereas protein synthesis remained intact. These data have demonstrated that vessel remodeling secondary to hypertension was characterized in part by nestin upregulation in vascular smooth muscle cells. The selective role of nestin in peptide growth factor-stimulated DNA synthesis has revealed that the proliferative and hypertrophic responses of vascular smooth muscle cells were mediated by divergent signaling events. nestin; carotid artery; aorta; hypertension; vascular remodeling DURING THE DEVELOPMENT of the central nervous system (CNS), a population of neuroepithelial stem cells was initially identified via expression of the intermediate filament protein nestin (8,18). Nestin is a 240-kDa protein and a member of the class VI family of intermediate filament proteins, and, in contrast to other classes, it is unable to self-assemble and form homodimers because of a short NH 2 terminus (37, 39). Therefore, nestin will form heterodimers with other intermediate filament proteins, including vimentin and desmin (37). The promoter region upstream of exon 1 of the nestin gene does not contain any identifiable elements regulating expression. However, the nestin gene does contain regulatory elements in the various intron regions that drive expression in a cell-specific manner (37). In neural progenitor/stem cells, nestin expression is independently regulated by restricted enhancer elements identified in the second intron (43). In humans, a highly conserved region that directed expression was also identified in the second intron of the nestin gene (21). However, nestin expression driven by the second intron was not limited to CNSresident stem cells, since a transgenic mouse containing the 5.8-kb fragment of the promoter region and the 1.8-kb fragment of the second intron of the rat nestin gene linked to the reporter green fluorescent protein (GFP) identified progenitor/ stem cell populations in the skin, skeletal mus...

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“…Still, many challenges remain and are currently being addressed, particularly with regard to the improvement of graft mechanical properties in a limited period. In order to develop a patent tissue-engineered blood vessel that grossly resembles native tissue, required culture times in most studies exceed 8 weeks [29, 30]. Tissue-engineered blood vessels are not likely to be used in emergency situations because of the time necessary to allow for cell expansion, extracellular matrix production and organization, and attainment of desired mechanical strength.…”

Section: Discussionmentioning

confidence: 99%

Tissue-Engineered Vessel Strengthens Quickly under Physiological Deformation: Application of a New Perfusion Bioreactor with Machine Vision

Ge²,

Zhou³

et al. 2005

J Vasc Res

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In order to develop a patent tissue-engineered blood vessel that grossly resembles native tissue, required culture times in most studies exceed 8 weeks. For the sake of shortening the maturation period of the constructs, we have used deformation as the basic index for mechanical environment control. A new bioreactor with a machine vision identifier was developed to accurately control the deformation of the construct during the perfusion process. Two groups of seeded constructs (n = 4 per group) were investigated in this study, with one group stimulated by a cyclic deformation of 10% and the other by a pulsatile pressure that gradually increased to 120 mm Hg (the control group). After 21 days of culture, the mechanical properties of the constructs were examined. The average burst strength and suture retention strength in the two groups were significantly different (t test, p < 0.05). For the experimental group, the average burst strength and suture retention strength were higher than those of the control group, by 31.6 and 23.4%, respectively. Specifically, the average burst strength of the constructs reached 1,402 mm Hg (close to that of the native vessel, i.e. 1,680 mm Hg) within a relatively short period of 21 days. In conclusion, deformation is an observable, controllable and very valuable index for mechanical environment control in vascular tissue engineering. It makes the control of mechanical stimuli more essential and experiments more comparable.

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Mechanical strain-induced human vascular matrix synthesis: The role of angiotensin II

Cited by 42 publications

References 19 publications

Candesartan cilexetil protects cavernous tissue in spontaneously hypertensive rats

Candesartan cilexetil protects cavernous tissue in spontaneously hypertensive rats

Nestin upregulation characterizes vascular remodeling secondary to hypertension in the rat

Tissue-Engineered Vessel Strengthens Quickly under Physiological Deformation: Application of a New Perfusion Bioreactor with Machine Vision

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