Flow (shear stress)-mediated remodeling of resistance arteries in diabetes

Vessières, Emilie; Freidja, Mohamed Lamine; Loufrani, Laurent; Fassot, Céline; Henrion, Didier

doi:10.1016/j.vph.2012.03.006

Cited by 37 publications

(42 citation statements)

References 77 publications

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“…Hence, while there was no overt remodelling, such as increased collagen deposition and large changes in wall thickness (Mulvany, 1999), there were changes to the vessel dimensions to accommodate their inability to respond appropriately to changes in flow, as reported in other mice models (Albinsson et al , 2007). There are reports of altered shear response in resistance arteries of diabetic and hypertensive rats (Matrougui et al , 1998; Bouvet et al , 2007; Belin de Chantemele et al , 2009; Vessieres et al , 2012; Dumont et al , 2014) where expression or glycosylation state of extracellular matrix molecules is commonly affected (Intengan & Schiffrin, 2000; Rauch et al , 2011; Bogdani et al , 2014). However, there has been no investigation of whether changes in shear response in such pathological vessels are associated with changes in laminin isoform expression, a possibility that requires future investigation.…”

Section: Discussionmentioning

confidence: 99%

Endothelial basement membrane laminin 511 is essential for shear stress response

Russo¹,

Luik²,

Yousif³

et al. 2016

The EMBO Journal

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Shear detection and mechanotransduction by arterial endothelium requires junctional complexes containing PECAM‐1 and VE‐cadherin, as well as firm anchorage to the underlying basement membrane. While considerable information is available for junctional complexes in these processes, gained largely from in vitro studies, little is known about the contribution of the endothelial basement membrane. Using resistance artery explants, we show that the integral endothelial basement membrane component, laminin 511 (laminin α5), is central to shear detection and mechanotransduction and its elimination at this site results in ablation of dilation in response to increased shear stress. Loss of endothelial laminin 511 correlates with reduced cortical stiffness of arterial endothelium in vivo, smaller integrin β1‐positive/vinculin‐positive focal adhesions, and reduced junctional association of actin–myosin II. In vitro assays reveal that β1 integrin‐mediated interaction with laminin 511 results in high strengths of adhesion, which promotes p120 catenin association with VE‐cadherin, stabilizing it at cell junctions and increasing cell–cell adhesion strength. This highlights the importance of endothelial laminin 511 in shear response in the physiologically relevant context of resistance arteries.

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Section: Discussionmentioning

confidence: 99%

Endothelial basement membrane laminin 511 is essential for shear stress response

Russo¹,

Luik²,

Yousif³

et al. 2016

The EMBO Journal

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“…Even though circulating nitrite levels at 24 h after reperfusion in UAtreated hyperemic rats were low, we cannot exclude that a potential blood flow increase due, at least in part, to a UA-derived nitration/nitrosation product during reperfusion might contribute to the flow (shear stress)-induced outward remodeling (36). It is possible that the UA-induced luminal expansion of the MCA prevents the secondary hypoperfusion described to take place after reactive hyperemia (34).…”

Section: Discussionmentioning

confidence: 92%

Middle cerebral artery remodeling following transient brain ischemia is linked to early postischemic hyperemia: A target of uric acid treatment

Onetti

Dantas

Pérez

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Ischemia impairs blood supply to the brain and reperfusion is important to restore cerebral blood flow (CBF) and rescue neurons from cell death. However, reperfusion can induce CBF values exceeding the basal values prior to ischemia. This hyperemic effect has been associated with a worse ischemic brain damage, albeit the mechanisms that contribute to infarct expansion are not clear. In this study, we investigated the influence of early postischemic hyperemia on brain damage and middle cerebral artery (MCA) properties, and the effect of treatment with the endogenous antioxidant uric acid (UA). The MCA was occluded for 90 min followed by 24 h reperfusion in adult male Sprague-Dawley rats. Cortical CBF increases at reperfusion beyond 20% of basal values were taken as indicative of hyperemia. UA (16 mg/kg) or vehicle (Locke's buffer) was administered i.v. 135 min after MCA occlusion.Hyperemic compared to non-hyperemic rats showed MCA wall thickening (sham: 22.4 ± 0.8 μm; non-hyperemic: 23.1 ± 1.2 μm; hyperemic: 27.8 ± 0.9 at 60 mmHg; P < 0.001, hyperemic vs. sham) involving adventitial cell proliferation, increased oxidative stress and interleukin-18, and more severe brain damage. Thus, MCA remodeling after ischemia/reperfusion takes place under vascular oxidative and inflammatory stress conditions linked to hyperemia. UA administration attenuated MCA wall thickening, induced passive lumen expansion, and reduced brain damage in hyperemic rats, though it did not increase brain UA concentration. We conclude that hyperemia at reperfusion following brain ischemia induces vascular damage that can be attenuated by administration of the endogenous antioxidant UA.

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“…A chronic increase in blood flow induces changes in structure and function of arterioles or resistance arteries with an increase in diameter and wall mass (hypertrophy) and improved endothelium-dependent dilation. 6,10,12,[27][28][29] This remodeling has a major role in growth, pregnancy, and exercising as well as in ischemic diseases. Indeed, it is important for collateral arteries growth after occlusion of a larger artery, and consequently it is essential for postischemic revascularization.…”

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confidence: 99%

Determinants of Flow-Mediated Outward Remodeling in Female Rodents

Tarhouni

Guihot

Vessières

et al. 2014

ATVB

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Objective-Flow (shear stress)-mediated outward remodeling (FMR) of resistance arteries is a key adaptive process allowing collateral growth after arterial occlusion but declining with age. 17-β-estradiol (E2) has a key role in this process through activation of estrogen receptor α (ERα). Thus, we investigated the impact of age and timing for estrogen efficacy on FMR. Approach and Results-Female rats, 3 to 18 months old, were submitted to surgery to increase blood flow locally in 1 mesenteric artery in vivo. High-flow and normal-flow arteries were collected 2 weeks later for in vitro analysis. Diameter increased by 27% in high-flow arteries compared with normal-flow arteries in 3-month-old rats. The amplitude of remodeling declined with age (12% in 18-month-old rats) in parallel with E2 blood level and E2 substitution failed restoring remodeling in 18-month-old rats. Ovariectomy of 3-, 9-, and 12-month-old rats abolished FMR, which was restored by immediate E2 replacement. Nevertheless, this effect of E2 was absent 9 months after ovariectomy. In this latter group, ERα and endothelial nitric oxide synthase expression were reduced by half compared with age-matched rats recently ovariectomized. FMR did not occur in ERα −/− mice, whereas it was decreased by 50% in ERα +/− mice, emphasizing the importance of gene dosage in high-flow remodeling. Conclusions-E2 deprivation, rather than age, leads to decline in FMR, which can be prevented by early exogenous E2.However, delayed E2 replacement was ineffective on FMR, underlining the importance of timing of this estrogen action. 15 The initial results suggested a negative impact of the treatment, leading to a worldwide reduction in the use of substitution therapies. Nevertheless, recent publications with a more detailed analysis of the data countermanded the initial conclusion. Interestingly, a major difference in the effect of hormones between younger and older women has been shown. Indeed, the treatment tended to confer coronary protection in women treated within 10 years after menopause, whereas a latter treatment may induce deleterious effects. 24 The mechanisms accounting for the impact of timing in the atheroprotective action of estrogens has been recently reviewed. 15 In particular, it has been described, in the atheroma plaque, a decreased ERα expression 16,25 and an increase in 27-hydroxycholesterol (27HC) production. 26 Indeed, 27HC is a competitive antagonist of ER action, which can counteract the protective action of 17-β-estradiol (E2). 26To better understand to which extent a timing effect also can impact the function of arterioles, we investigated FMR of resistance arteries in young and old female rats and then in young ovariectomized rats as a model of surgical menopause. Materials and MethodsMaterials and Methods are available in the online-only Supplement. Results Estradiol Blood Level and FMRFourteen days after arterial ligation, arterial diameter was determined in vitro in response to stepwise increases in intraluminal pressure. Passive arterial diamet...

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Flow (shear stress)-mediated remodeling of resistance arteries in diabetes

Cited by 37 publications

References 77 publications

Endothelial basement membrane laminin 511 is essential for shear stress response

Endothelial basement membrane laminin 511 is essential for shear stress response

Middle cerebral artery remodeling following transient brain ischemia is linked to early postischemic hyperemia: A target of uric acid treatment

Determinants of Flow-Mediated Outward Remodeling in Female Rodents

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