Physical training and hypertension have opposite effects on endothelial brain-derived neurotrophic factor expression

Prigent‐Tessier, Anne; Quirié, Aurore; Maguin‐Gaté, Katy; Szostak, Justyna; Mossiat, Claude; Nappey, Maude; Devaux, Sylvie; Marie, Christine; Demougeot, Céline

doi:10.1093/cvr/cvt219

Cited by 74 publications

(82 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Authors suggested new perspectives on the role of endothelial BDNF in cardiovascular health. 22 Our conclusions suffer from the small size of our study group (n ¼ 31). The presented P values were not corrected for multiple comparisons and we could not perform reliable multivariate analysis.…”

Section: Discussionmentioning

confidence: 73%

Insulin resistance and brain-derived neurotrophic factor levels in chronic kidney disease

et al. 2014

View full text Add to dashboard Cite

Introduction: Insulin resistance is a frequent abnormality in chronic kidney disease (CKD) appearing in early stages. Factors known to promote insulin resistance in CKD patients include disorders of ion and acid-base equilibrium and circulating uremia toxins. Recent research has focused on the central nervous system as the source of the brain-derived neurotrophic factor (BDNF). The aim of our work was to study plasma BDNF concentrations in stage 3 and 4 CKD patients in relationship with insulin resistance and distribution of adipose tissue. Method: Plasma BDNF concentrations were measured in a study group of 31 patients, including a subgroup of 20 nondiabetic subjects. Additionally dual-energy X-ray absorptiometry (DXA) was performed. Homeostatic model assessment of insulin resistance (HOMA-IR) and homeostatic model assessment of B-cell function (HOMA-beta) indices were calculated. Results: Two separate analyses were performed. In the first analysis performed in all 31 CKD patients, there were no correlations between BDNF and: body mass index (BMI), android, gynoid fat distribution, HOMA-IR and HOMA-beta. In the second analysis performed in 20 CKD patients without diabetes, BDNF was negatively related to gynoid fat (Rs ¼ À0.47, P ¼ 0.034) and women revealed significantly lower levels of BDNF than men (P ¼ 0.046). Normotensive patients disclosed significantly higher BDNF levels than hypertensive patients in the whole CKD group (P ¼ 0.039) and in the non-diabetic subgroup (P ¼ 0.028). No correlations between BDNF and eGFR were found. Conclusions: Female sex and arterial hypertension are associated with lower BDNF plasma concentration in CKD patients.

show abstract

Section: Discussionmentioning

confidence: 73%

Insulin resistance and brain-derived neurotrophic factor levels in chronic kidney disease

et al. 2014

View full text Add to dashboard Cite

show abstract

“…It has been reported that the level of plasma BDNF decreased in the aged 16 and patients with CAD. 17 Consistently, decreased BDNF expression in vascular endothelium was associated with hypertension, 18 a common complication of CAD. Reduced TrkB expression in tissues was also found during aging.…”

Section: Discussionmentioning

confidence: 84%

Tyrosine Kinase Receptor B Protects Against Coronary Artery Disease and Promotes Adult Vasculature Integrity by Regulating Ets1-Mediated VE-Cadherin Expression

Jiang

Huang

et al. 2015

ATVB

View full text Add to dashboard Cite

Objective-Tyrosine kinase receptor B (TrkB) is a high-affinity receptor for brain-derived neurotrophic factor. In addition to its nervous system functions, TrkB is also expressed in the cardiovascular system. However, the association of TrkB and coronary artery disease (CAD) remains unknown. We investigated the role of TrkB in the development of CAD and its mechanism. Approach and Results-We performed a case-control study in 2 independent cohort of Chinese subjects and found -69C>G polymorphisms of TrkB gene significantly associated with CAD. TrkB -69C homozygotes, which corresponded to decreased TrkB expression by luciferase reporter assay, showed increased risk for CAD. Immunofluorescence analysis revealed that TrkB was expressed in the aortic endothelium in atherosclerotic lesions in humans and ApoE -/-mice. TrkB knockdown in the aortic endothelium resulted in vascular leakage in ApoE -/-mice. Mechanistic studies showed that TrkB regulated vascular endothelial cadherin (VE-cadherin) expression through induction and activation of Ets1 transcriptional factor. Importantly, TrkB activation attenuated proatherosclerotic factors induced-endothelial hyperpermeability in human vascular endothelial cells.Conclusions-Our data demonstrate that TrkB protects endothelial integrity during atherogenesis by promoting Ets1-mediated VE-cadherin expression and plays a previously unknown protective role in the development of CAD. Table). This difference was also observed in the Shanxi group (all P<0.05; Table). Multiple logistic regression analysis revealed homozygous TrkB -69C, rather than TrkB -69G carriers, were associated with an increased risk of CAD in the Shandong group (odds ratio, 2.1; 95% confidence interval, 1.68-2.62; P<0.01) and in the Shanxi group (odds ratio, 2.0; 95% confidence interval, 1.69-2.67; P<0.01), after adjusting sex, age, and body mass index. There was no association between the TrkB IVS13+40G>A polymorphism and CAD (P>0.05; Table). All genotype frequencies showed Hardy-Weinberg equilibrium. Statistical powers are all 100% in Shandong and Shanxi group. The clinical characteristics of the 2 cohorts of patients and controls are shown in Table I in the online-only Data Supplement.Polymorphism -69C>G is located in the promoter region of TrkB. It has been reported that approximately one third of promoter variants may alter gene expression to a functionally relevant extent. 8 We then constructed luciferase reporter vectors with TrkB promoter segments (-3258 to -11 bp) of contrasting genotypes (-69CC versus -69GG; Figure 1A and 1B) and tested the effect of TrkB -69C>G polymorphism on luciferase reporter gene expression. Regardless of genotype, the promoter significantly promoted luciferase expression ( Figure 1C and 1D). Of note, luciferase activity was significantly lower with the -69C construct than with the -69G construct in HeLa cells and human vascular endothelial cells (ECs; Figure 1C and 1D). These data suggested that decreased TrkB expression might be associated with increased risk for CAD. TrkB is...

show abstract

“…Corresponding sedentary rats were kept in their housing cage that was placed at the proximity of the treadmill apparatus. We previously showed that such a modality of physical training (treadmill activity with a horizontal position, 30 minutes/day, 18 m/minute, for 7 consecutive days) induced a mild increase in citrate synthase activity in skeleton muscles, did not change blood pressure in WKY rats and SHR, 13 and resulted in a twofold increase in mature BDNF levels in the cortex when induced in control Wistar rats. 14 …”

Section: Physical Trainingmentioning

confidence: 99%

Brain BDNF Levels Elevation Induced by Physical Training is Reduced after Unilateral Common Carotid Artery Occlusion in Rats

Banoujaafar

Hoecke

Mossiat

et al. 2014

J Cereb Blood Flow Metab

Self Cite

View full text Add to dashboard Cite

We investigated the contribution of blood flow elevation in the cerebrovasculature to physical training-induced brain-derived neurotrophic factor (BDNF) levels elevation in the brain. Brain-derived neurotrophic factor protein levels were measured in the motor cortex 24 h after the last session of a forced treadmill walking (30 minutes a day, 18 m/minute for 7 consecutive days). Unilateral common carotid artery occlusion and modulation of exercise intensity (0 versus À 10% inclination of the treadmill) were used as strategies to reduce the (normal) elevation of flow in the cerebrovasculature occurring during exercise. Administration of N-nitro-L-arginine methyl ester (L-NAME, 60 mg/kg before each exercise sessions) and genetic hypertension (spontaneously hypertensive rats) were used as approaches to reduce stimulation of nitric oxide production in response to shear stress elevation. Vascular occlusion totally and partially abolished the effect of physical training on BDNF levels in the hemisphere ipsilateral and contralateral to occlusion, respectively. BDNF levels were higher after high than low exercise intensity. In addition, both genetic hypertension and L-NAME treatment blunted the effects of physical training on BDNF. From these results, we propose that elevation of brain BDNF levels elicited by physical training involves changes in cerebral hemodynamics.

show abstract

Physical training and hypertension have opposite effects on endothelial brain-derived neurotrophic factor expression

Abstract: Cardiovascular BDNF is mainly localized within endothelial cells in which its expression is dependent on endothelial function. These results open new perspectives on the role of endothelial BDNF in cardiovascular health.

Cited by 74 publications

References 44 publications

Insulin resistance and brain-derived neurotrophic factor levels in chronic kidney disease

Insulin resistance and brain-derived neurotrophic factor levels in chronic kidney disease

Tyrosine Kinase Receptor B Protects Against Coronary Artery Disease and Promotes Adult Vasculature Integrity by Regulating Ets1-Mediated VE-Cadherin Expression

Brain BDNF Levels Elevation Induced by Physical Training is Reduced after Unilateral Common Carotid Artery Occlusion in Rats

Contact Info

Product

Resources

About