Secondhand smoke exposure induces Raf/ERK/MAPK-mediated upregulation of cerebrovascular endothelin ETA receptors

Cao, Lei; Xu, Cang‐Bao; Zhang, Yaping; Cao, Yunxia; Edvinsson, Lars

doi:10.1186/1471-2202-12-109

Cited by 28 publications

(22 citation statements)

References 37 publications

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“…Contrary to endothelin 1, there was no contractile response to sarafotoxin 6c in ischemic cerebral arteries from hypertensive rats indicating no contractile response of endothelin B receptors. The contractile responses to endothelin 1 and sarafotoxin 6c correlate with previous results in the cerebral arteries from rats exposed to second-hand smoke, which is another risk factor for stroke [18]. These rats were not subjected to stroke, but in combination with our results they suggest that risk factors for stroke have an effect on the vasocontractile receptor responses in cerebral arteries, since there was no change in the vasocontractile receptor responses in ischemic cerebral arteries from WKY rats (normotensive rats).…”

Section: Discussionsupporting

confidence: 84%

Contractile Responses in Spontaneously Hypertensive Rats after Transient Middle Cerebral Artery Occlusion

et al. 2017

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Stroke is one of the leading causes of mortality and morbidity worldwide, and few therapeutic treatments have shown beneficial effect clinically. One reason for this could be the lack of risk factors incorporated into the preclinical stroke research. We have previously demonstrated phenotypic receptor changes to be one of the injurious mechanisms occurring after stroke but mostly in healthy rats. The aim of this study was to investigate if hypertension has an effect on vasoconstrictive receptor responses to endothelin 1, sarafotoxin 6c and angiotensin II after stroke by inducing transient middle cerebral artery occlusion in spontaneously hypertensive rats and Wistar-Kyoto rats using the wire-myograph. We demonstrated an increased contractile response to endothelin 1 and extracellular potassium as well as an increased carbachol-induced dilator response in the middle cerebral arteries from hypertensive rats after stroke. This study demonstrates the importance of including risk factors in experimental stroke research.

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Section: Discussionsupporting

confidence: 84%

Contractile Responses in Spontaneously Hypertensive Rats after Transient Middle Cerebral Artery Occlusion

et al. 2017

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“…(a) One-way analysis of variance (ANOVA) between lifetime nonsmokers, current smokers, and former smokers; green diamonds vertically centered on mean spanning 1 SD; horizontal width proportional to sample size; mean CT as follows: nonsmokers, 181±65, n ¼ 80; current smokers, 147±61, n ¼ 10; former smokers, 149 ± 64 mm, n ¼ 57; P ¼ 0.011; (b) Two-sample t-test subgroup analysis of patients with drusen or early AMD; mean CT is as follows: nonsmokers, 146 ± 46 mm, n ¼ 49; history of smoking, 121 ± 41 mm, n ¼ 49; P ¼ 0.006. exposure. 41 Smoking appears to impair endothelial cell function in many vascular regions, and evidence supports long-term vasoconstriction and altered endothelial response 37,42,43 to various vasoactive mediators in tobacco smoke. 40,44,45 Human studies indicate abnormal choroidal vascular reactivity to carbogen (high oxygen) inhalation in chronic smokers.…”

Section: Discussionmentioning

confidence: 97%

Smoking and choroidal thickness in patients over 65 with early-atrophic age-related macular degeneration and normals

Sigler

Randolph

Calzada

et al. 2014

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Objective To compare macular choroidal thickness between cigarette smokers, those with a history of smoking, and nonsmokers in patients over 65 years of age with earlyatrophic age-related macular degeneration (AMD) and normals. Methods Prospective, consecutive, observational case series. Enhanced depth imaging spectral domain optical coherence tomography 12-line radial scans were performed and choroidal thickness manually quantified at 84 points in the central 3 mm of the macula. Data of normals, soft drusen alone, and soft drusen with additional features of early AMD were compared. A multivariate analysis of variance (MANOVA) model, controlling for age, was constructed to evaluate the effect of smoking history and AMD features on choroidal thickness. Results A history of smoking was significantly associated with a thinner choroid across all patients via logistic regression (P ¼ 0.004; O.R. ¼ 12.4). Mean macular choroidal thickness was thinner for smokers (148±63 mm) than for nonsmokers (181±65 mm) among all diagnosis categories (P ¼ 0.003). Subgroup analysis of patients with AMD features revealed a similar decreased choroidal thickness in smokers (121 ± 41 mm) compared with nonsmokers (146 ± 46 mm, P ¼ 0.006). Bivariate analysis revealed an association between increased pack-years of smoking and a thin choroid across all patients (Po0.001) and among patients with features of early AMD (Po0.001). Both the presence of features of macular degeneration (Po0.001) and a history of smoking (P ¼ 0.024) were associated with decreased choroidal thickness in a MANOVA model. ConclusionChronic cigarette smoke exposure may be associated with decreased choroidal thickness. There may be an anatomic sequelae to chronic tobacco smoke exposure that underlies previously reported AMD risk.

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“…[104][105][106] In this line, accumulating evidence revealed an adverse impact of TS on cerebrovascular system leading to a substantial increase of the risk for ischemic stroke, silent cerebral infarctions, vascular dementia, and incidence of other major CNS disorders (including Alzheimer's disease). [107][108][109][110] Striking lines of evidence have established a significant link between smoking and pathophysiology of BBB endothelial dysfunction. [111][112][113] As shown in Figure 4, a acute or chronic TS exposure significantly elevates endothelial oxidative and nitrosative stress responses resulting in a progressive loss of BBB integrity.…”

Section: Smoking and Cerebrovascular Complications: Does Nicotine Havmentioning

confidence: 99%

Drugs of abuse and blood-brain barrier endothelial dysfunction: A focus on the role of oxidative stress

Sajja

Rahman

Cucullo

2015

J Cereb Blood Flow Metab

119

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Psychostimulants and nicotine are the most widely abused drugs with a detrimental impact on public health globally. While the long-term neurobehavioral deficits and synaptic perturbations are well documented with chronic use of methamphetamine, cocaine, and nicotine, emerging human and experimental studies also suggest an increasing incidence of neurovascular complications associated with drug abuse. Short-or long-term administration of psychostimulants or nicotine is known to disrupt blood-brain barrier (BBB) integrity/function, thus leading to an increased risk of brain edema and neuroinflammation. Various pathophysiological mechanisms have been proposed to underlie drug abuse-induced BBB dysfunction suggesting a central and unifying role for oxidative stress in BBB endothelium and perivascular cells. This review discusses drug-specific effects of methamphetamine, cocaine, and tobacco smoking on brain microvascular crisis and provides critical assessment of oxidative stress-dependent molecular pathways focal to the global compromise of BBB. Additionally, given the increased risk of human immunodeficiency virus (HIV) encephalitis in drug abusers, we have summarized the synergistic pathological impact of psychostimulants and HIV infection on BBB integrity with an emphasis on unifying role of endothelial oxidative stress. This mechanistic framework would guide further investigations on specific molecular pathways to accelerate therapeutic approaches for the prevention of neurovascular deficits by drugs of abuse.

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Secondhand smoke exposure induces Raf/ERK/MAPK-mediated upregulation of cerebrovascular endothelin ETA receptors

Cited by 28 publications

References 37 publications

Contractile Responses in Spontaneously Hypertensive Rats after Transient Middle Cerebral Artery Occlusion

Contractile Responses in Spontaneously Hypertensive Rats after Transient Middle Cerebral Artery Occlusion

Smoking and choroidal thickness in patients over 65 with early-atrophic age-related macular degeneration and normals

Drugs of abuse and blood-brain barrier endothelial dysfunction: A focus on the role of oxidative stress

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