Patients at High Risk of Cerebrovascular Disease: The REACH Study

Mostaza, J.M.; Martín-Jadraque, Raquel; Vicente, Ignacio; Nieto-Martín, María Dolores; Lahoz, Carlos H.

doi:10.1159/000200443

Cited by 12 publications

(9 citation statements)

References 59 publications

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“…Therefore, the damage of CS not only limits to lung tissue but also vascular system. CS is a known risk factor not only for peripheral cardiovascular inflammation-related diseases [2,3] but also for cerebrovascular diseases, such as stroke [4]. …”

Section: Introductionmentioning

confidence: 99%

“…Interestingly, CS or chemicals present in CS have been shown to induce HO-1 expression in various cell types [7-10] including cerebral endothelial cells [11]. Therefore, PPCSE-induced HO-1 expression in cerebral vessels might be an important factor for brain injury in hemorrhagic stroke which incident rate has been correlated with cigarette smoking previously [4]. …”

Section: Introductionmentioning

confidence: 99%

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Cigarette smoke extract upregulates heme oxygenase-1 via PKC/NADPH oxidase/ROS/PDGFR/PI3K/Akt pathway in mouse brain endothelial cells

Shih

Cheng

Hsiao

et al. 2011

J Neuroinflammation

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BackgroundIn the brain, the inducible form of heme oxygenase (HO-1) has been recently demonstrated to exacerbate early brain injury produced by intracerebral hemorrhagic stroke which incident rate has been correlated with cigarette smoking previously. Interestingly, cigarette smoke (CS) or chemicals present in CS have been shown to induce HO-1 expression in various cell types, including cerebral endothelial cells. However, the mechanisms underlying CS modulating HO-1 protein expression are not completely understood in the brain vessels.ObjectiveThe aim of the present study was to investigate the mechanisms underlying CS modulating HO-1 protein expression in cerebral endothelial cells.MethodsCultured cerebral endothelial cells (bEnd.3) were used to investigate whether a particulate phase of cigarette smoke extract (PPCSE) regulates HO-1 expression and to investigate the molecular mechanisms involved in HO-1 expression in bEnd.3 cells.ResultsWe demonstrated that PPCSE (30 μg/ml) significantly induced HO-1 protein expression and its enzymatic activity in bEnd.3 cells determined by western blotting and bilirubin formation, respectively. PPCSE-induced HO-1 expression was mediated through phosphatidylcholine phospholipase C (PC-PLC), PKCδ, and PI3K/Akt which were observed by pretreatment with their respective pharmacological inhibitors or transfection with dominant negative mutants of PKCδ and Akt. ROS scavenger (N-acetyl-L-cysteine, NAC) blocked the PPCSE-induced ROS generation and HO-1 expression. Pretreatment with selective inhibitors of PKCδ (rottlerin) and NADPH oxidase [diphenyleneiodonium chloride (DPI) and apocynin (APO)] attenuated the PPCSE-induced NADPH oxidase activity, ROS generation, and HO-1 expression. In addition, we found that PPCSE induced PI3K/Akt activation via NADPH oxidase/ROS-dependent PDGFR phosphorylation.ConclusionsTaken together, these results suggested that PPCSE-induced HO-1 expression is mediated by a PC-PLC/PKCδ/NADPH oxidase-dependent PDGFR/PI3K/Akt pathway in bEnd.3 cells.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cigarette smoke extract upregulates heme oxygenase-1 via PKC/NADPH oxidase/ROS/PDGFR/PI3K/Akt pathway in mouse brain endothelial cells

Shih

Cheng

Hsiao

et al. 2011

J Neuroinflammation

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“…This is of clinical relevance as the expression of ApoE and LDL receptors differs in young adult versus old rats following cerebral ischemia [47]. Atherosclerosis is an important risk factor in patients with ischemia [48]. Therefore, consideration of this pathology in animal stroke models is crucial.…”

Section: Atherosclerosismentioning

confidence: 99%

Are Underlying Assumptions of Current Animal Models of Human Stroke Correct: from STAIRs to High Hurdles?

Turner

Jickling

Sharp

2011

Transl. Stroke Res.

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Animal models of acute ischemic stroke have been criticized for failing to translate to human stroke. Nevertheless, animal models are necessary to improve our understanding of stroke pathophysiology and to guide the development of new stroke therapies. The rabbit embolic clot model is one animal model that has led to an effective therapy in human acute ischemic stroke, namely tissue plasminogen activator (tPA). We propose that potential compounds that demonstrate efficacy in non-rabbit animal models of acute ischemic stroke should also be tested in the rabbit embolic blood clot model and, where appropriate, compared to tPA prior to investigation in humans. Furthermore, the use of anesthesia needs to be considered as a major confounder in animal models of acute ischemic stroke, and death should be included as an outcome measure in animal stroke studies. These steps, along with the current STAIRs recommendations, may improve the successful translation of experimental therapies to clinical stroke treatments.

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“…The international Reduction of Atherothrombosis for Continued Health (REACH) registry of 67,888 patients with symptomatic atherothrombotic disease showed that 41% of patients with stroke/TIA (18,843 patients with predominantly non-cardiogenic ischaemic stroke) also had disease in at least one additional vascular territory [5,10,11]. Patients with documented polyVD have more than double the risk of a major event or hospitalisation at 1 year compared with patients in whom only the cerebral territory is involved (fig.…”

Section: Stroke Patients With Polyvd: a High-risk Populationmentioning

confidence: 99%

Challenges to the Management of High-Risk Stroke Patients with Multiple-Site Occlusive Vascular Disease

Sander¹,

Carolei

Diehm

et al. 2011

Cerebrovasc Dis

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Stroke patients are at high risk of secondary vascular events. Although in the short term the risk of experiencing a second stroke is high, in the long term patients are more likely to have myocardial infarction. Many stroke patients have also developed polyvascular disease in the form of coronary artery disease and peripheral arterial disease, which is a marker of increased morbidity and mortality in patients with non-cardioembolic ischemic stroke. Despite the high risk of events in these patients, current evidence-based guidelines make very few recommendations that address the need to detect and manage polyvascular disease following a stroke. Optimised Stroke Care for Re-Admission Reduction in Europe (OSCARE) is an initiative that has been set up to address some of these shortcomings.

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Patients at High Risk of Cerebrovascular Disease: The REACH Study

Cited by 12 publications

References 59 publications

Cigarette smoke extract upregulates heme oxygenase-1 via PKC/NADPH oxidase/ROS/PDGFR/PI3K/Akt pathway in mouse brain endothelial cells

Cigarette smoke extract upregulates heme oxygenase-1 via PKC/NADPH oxidase/ROS/PDGFR/PI3K/Akt pathway in mouse brain endothelial cells

Are Underlying Assumptions of Current Animal Models of Human Stroke Correct: from STAIRs to High Hurdles?

Challenges to the Management of High-Risk Stroke Patients with Multiple-Site Occlusive Vascular Disease

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