Acute hypertension induces brain injury and blood–brain barrier disruption through reduction of claudins mRNA expression in rat

Mohammadi, Mohammad Taghi; Dehghani, Gholam Abbas

doi:10.1016/j.prp.2014.05.007

Cited by 43 publications

(36 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…indicated that the “fence” function of the TJ proteins is disturbed in endothelial cells of rats by showing that claudin‐1 and claudin‐5 structure is significantly more impaired in the hypertensive rats as compared to age‐matched rats . Similarly, Mohammadi and Dehghani found that the expression of claudin‐3, claudin‐5 and claudin‐12 mRNA decreased in response to hypertension, and that there was a relationship between reduction of claudins mRNA levels and BBB permeability in rats …”

Section: Discussionmentioning

confidence: 92%

Association of genetic polymorphisms of claudin‐1 with small vessel vascular dementia

Srinivasan

Braidy

et al. 2017

Clin Exp Pharma Physio

View full text Add to dashboard Cite

The most recent hypothesis of the development of small vessel vascular dementia (VaD) emphasises the role of blood-brain barrier (BBB) dysfunction. It is hypothesised that certain genetic polymorphisms of the BBB tight junction claudin-1 protein, in combination with adverse environmental risk factors, increase the risk of BBB dysfunction and small vessel VaD. In this case-control study, 97 control participants, with a mean Mini Mental State Exam (MMSE) score of 29.1, and 38 VaD participants were recruited and completed a questionnaire on their medical history and lifestyle factors. Blood was also collected and two single nucleotide polymorphisms (SNPs), rs17501010 and rs893051 of claudin-1 genotyping, were analysed by real-time polymerase chain reaction (PCR) assay. A significantly higher frequency of all rs893051 SNP genotypes (GC and CC) was found in the VaD population (OR=4.8, P=0.006 and OR=6, P<0.001 respectively). Patients with TT genotype of rs17501010 were also more likely to have VaD (OR=3.25, P=0.022). Stratification analysis revealed that having combined haplotype GC+CC of rs893051 and lipid disorders was associated with higher risk of VaD (OR=9.9, P<0.001). For patients with type 2 diabetes the odds ratio of VaD increased significantly in GC+CC genotypes of rs893051 (OR=12.57, P<0.0001) and GT+TT of rs17501010 (OR=5.33, P=0.01).

show abstract

Section: Discussionmentioning

confidence: 92%

Association of genetic polymorphisms of claudin‐1 with small vessel vascular dementia

Srinivasan

Braidy

et al. 2017

Clin Exp Pharma Physio

View full text Add to dashboard Cite

show abstract

“…Multiple lines of evidence indicate that an imbalance of ROS production and elimination (also known as oxidative stress) in the brain cause sympathoexcitation, contributing to arterial hypertension in SHR, salt‐induced hypertension, experimental jet lag and renovascular models (two‐kidney one‐clip) . Thus, in the present study we analysed, at the transcriptional and functional levels, whether an imbalance between pro‐oxidant and antioxidant capacity in the medulla would be associated with hypertension in adult rats subjected to perinatal protein restriction.…”

Section: Discussionmentioning

confidence: 99%

“…The sympathetic nervous system is regulated by different sites into the brainstem, especially by the neurons located in the ventral medulla, 7,22 which determine the central sympathetic outflow and also by the neurons located in dorsal medulla, which receive inputs from peripheral baroreceptors and chemoreceptors, regulating the presympathetic neuron activity of the ventral medulla. 5,7,23 Multiple lines of evidence indicate that an imbalance of ROS production and elimination (also known as oxidative stress) in the brain cause sympathoexcitation, 15,[24][25][26] contributing to arterial hypertension in SHR, 15 salt-induced hypertension, 27 experimental jet lag 28 and renovascular models (two-kidney one-clip). 29 Thus, in the present study we analysed, at the transcriptional and functional levels, whether an imbalance between pro-oxidant and antioxidant capacity in the medulla would be associated with hypertension in adult rats subjected to perinatal protein restriction.…”

Section: Discussionmentioning

confidence: 99%

Maternal protein restriction induced‐hypertension is associated to oxidative disruption at transcriptional and functional levels in the medulla oblongata

Alves

Oliveira

Ferreira

et al. 2016

Clin Exp Pharma Physio

View full text Add to dashboard Cite

Maternal protein restriction during pregnancy and lactation predisposes the adult offspring to sympathetic overactivity and arterial hypertension. Although the underlying mechanisms are poorly understood, dysregulation of the oxidative balance has been proposed as a putative trigger of neural-induced hypertension. The aim of the study was to evaluate the association between the oxidative status at transcriptional and functional levels in the medulla oblongata and maternal protein restriction induced-hypertension. Wistar rat dams were fed a control (normal protein; 17% protein) or a low protein ((Lp); 8% protein) diet during pregnancy and lactation, and male offspring was studied at 90 days of age. Direct measurements of baseline arterial blood pressure (ABP) and heart rate (HR) were recorded in awakened offspring. In addition, quantitative RT-PCR was used to assess the mRNA expression of superoxide dismutase 1 (SOD1) and 2 (SOD2), catalase (CAT), glutathione peroxidase (GPx), Glutamatergic receptors (Grin1, Gria1 and Grm1) and GABA(A)-receptor-associated protein like 1 (Gabarapl1). Malondialdehyde (MDA) levels, CAT and SOD activities were examined in ventral and dorsal medulla. Lp rats exhibited higher ABP. The mRNA expression levels of SOD2, GPx and Gabarapl1 were down regulated in medullary tissue of Lp rats (P<.05, t test). In addition, we observed that higher MDA levels were associated to decreased SOD (approximately 45%) and CAT (approximately 50%) activities in ventral medulla. Taken together, our data suggest that maternal protein restriction induced-hypertension is associated with medullary oxidative dysfunction at transcriptional level and with impaired antioxidant capacity in the ventral medulla.

show abstract

“…Animal studies suggest that such a pattern is consistent with myelin damage 26 . However, mechanisms by which hypertension affects brain white matter are varied and complex 1,27,28 . Chronic hypertension is associated with vascular remodeling and reduced vascular reserve, which may lead to ischemia.…”

Section: Discussionmentioning

confidence: 99%

“…Chronic hypertension is associated with vascular remodeling and reduced vascular reserve, which may lead to ischemia. Hypertension also interferes with perivascular lymphatic drainage and increases blood-brain permeability, resulting in fluid accumulation that may be toxic to cells 28 . Both tissue damage and fluid accumulation will alter diffusion.…”

Section: Discussionmentioning

confidence: 99%

Hypertension-Related Alterations in White Matter Microstructure Detectable in Middle Age

et al. 2015

View full text Add to dashboard Cite

Most studies examining associations between hypertension and brain white matter microstructure have focused on older adults or on cohorts with a large age range. Since hypertension effects on the brain may vary with age it is important to focus on middle age, when hypertension becomes more prevalent. We used linear mixed effect models to examine differences in white matter diffusion metrics as a function of hypertension in a well-characterized cohort of middle-aged men (N=316, mean 61.8 years; range 56.7–65.6). Diffusion metrics were examined in nine tracts reported to be sensitive to hypertension in older adults. Relative to normotensive individuals, individuals with longstanding hypertension (> 5.6 years) showed reduced fractional anisotropy or increased diffusivity in most tracts. Effects were stronger among carriers than non-carriers of the apolipoprotein E ε4 allele for two tracts connecting frontal regions with other brain areas. Significant differences were observed even after adjustment for potentially-related lifestyle and cardiovascular risk factors. Shorter duration of hypertension or better blood pressure control among hypertensive individuals did not lessen the adverse effects. These findings suggest that microstructural white matter alterations appear early in the course of hypertension and may persist despite adequate treatment. Although longitudinal studies are needed to confirm these findings, the results suggest that prevention—rather than management—of hypertension may be vital to preserving brain health in aging.

show abstract

Acute hypertension induces brain injury and blood–brain barrier disruption through reduction of claudins mRNA expression in rat

Cited by 43 publications

References 32 publications

Association of genetic polymorphisms of claudin‐1 with small vessel vascular dementia

Association of genetic polymorphisms of claudin‐1 with small vessel vascular dementia

Maternal protein restriction induced‐hypertension is associated to oxidative disruption at transcriptional and functional levels in the medulla oblongata

Hypertension-Related Alterations in White Matter Microstructure Detectable in Middle Age

Contact Info

Product

Resources

About