Tight junction proteins of cerebral endothelial cells in early postnatal development

Кувачева, Н. В.; Моргун, А. В.; Malinovskaya, N. A.; Gorina, Ya. V.; Хилажева, Е. Д.; Пожиленкова, Е. А.; Panina, Yu. A.; Boytsova, E. B.; Ruzaeva, V A; Труфанова, Л. В.; Салмина, А. Б.

doi:10.1134/s1990519x16050084

Cited by 9 publications

(4 citation statements)

References 20 publications

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“…Indeed, two of these experimental studies have explicitly linked ELS to behavioral phenotypes associated with depression in adulthood through this neuroinflammatory pathway (Réus et al, ; Wang et al, ) and one showed that the behavioral phenotype associated with depression could be resolved with pharmacological agents that blocked microglia activation (Wang et al, ). ELS may also lead to greater permeability of the BBB (Kuvacheva et al, ), which allows more peripheral inflammatory cytokines and cells to access the CNS. Indeed, experimental animal models have shown that vulnerability to the behavioral effects of stress are linked to greater permeability in the BBB (Menard et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Increased sensitivity of the CNS to peripheral inflammatory activity could occur through several mechanisms. These include increasing the permeability of the blood–brain barrier (BBB) (Kuvacheva et al, ; Menard et al, ) and increasing the size, density, and proinflammatory sensitivity of microglia, the resident inflammatory cells in the brain (Bilbo & Schwarz, ; Calcia et al, ; Delpech et al, ; Réus et al, ; Wang et al, ). Importantly, in both of these cases, individuals with a history of ELS would experience more neuroinflammation following the same peripheral stimulus, leading to more profound psychological and behavioral changes.…”

Section: Introductionmentioning

confidence: 99%

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Early life stress sensitizes individuals to the psychological correlates of mild fluctuations in inflammation

Kuhlman

Robles

Haydon

et al. 2019

Developmental Psychobiology

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Background Early life stress (ELS) has been linked to health disparities across the human lifespan, particularly increased risk for depression and its recurrence. In this study we explore two plausible and competing pathways through which ELS may lead to depression via inflammation. Methods Participants (ages 18–22; n = 41) completed the Early Trauma Inventory as a measure of ELS. Participants then completed consecutive daily diaries of mood and other sickness behavior for the 7 days prior to and 7 days after receiving the annual influenza vaccine. Circulating concentrations of plasma interleukin‐6 (IL‐6) were measured immediately before and 24 hr after vaccination. Results ELS was not associated with the magnitude of change in IL‐6 from pre‐ to post‐vaccine, however, exposure to ELS moderated the association between change in IL‐6 from pre‐ to post‐vaccine and changes in both cognitive difficulty and depressed mood. Individuals exposed to greater ELS showed greater psychological sensitivity to increases in IL‐6. Conclusions Exposure to ELS may increase sensitivity to peripheral inflammation in the central nervous system. Future studies elaborating on the impact of ELS on the sensitivity of specific neural circuits and cells to inflammation are needed.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Early life stress sensitizes individuals to the psychological correlates of mild fluctuations in inflammation

Kuhlman

Robles

Haydon

et al. 2019

Developmental Psychobiology

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“…Using BMECs but not ECs of other origin as a part of the models is more physiological to reproduce the main mechanisms of BBB development and functioning. As we have shown before, specific metabolic properties of BMECs makes them an interesting object for managing the barrier permeability in BBB models, or even in tissue models based on the cerebral endothelial monolayer (i.e., neurogenic niche in vitro model) [ 123 , 139 , 140 , 141 , 142 , 143 , 144 ].…”

Section: Application Of In Vitro Nvu/bbb Models For Studying Mitochondria-related Changes In Cell Metabolism: Current Trends and Challengmentioning

confidence: 99%

Blood–Brain Barrier and Neurovascular Unit In Vitro Models for Studying Mitochondria-Driven Molecular Mechanisms of Neurodegeneration

Салмина

Kharitonova

Gorina

et al. 2021

IJMS

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Pathophysiology of chronic neurodegeneration is mainly based on complex mechanisms related to aberrant signal transduction, excitation/inhibition imbalance, excitotoxicity, synaptic dysfunction, oxidative stress, proteotoxicity and protein misfolding, local insulin resistance and metabolic dysfunction, excessive cell death, development of glia-supported neuroinflammation, and failure of neurogenesis. These mechanisms tightly associate with dramatic alterations in the structure and activity of the neurovascular unit (NVU) and the blood–brain barrier (BBB). NVU is an ensemble of brain cells (brain microvessel endothelial cells (BMECs), astrocytes, pericytes, neurons, and microglia) serving for the adjustment of cell-to-cell interactions, metabolic coupling, local microcirculation, and neuronal excitability to the actual needs of the brain. The part of the NVU known as a BBB controls selective access of endogenous and exogenous molecules to the brain tissue and efflux of metabolites to the blood, thereby providing maintenance of brain chemical homeostasis critical for efficient signal transduction and brain plasticity. In Alzheimer’s disease, mitochondria are the target organelles for amyloid-induced neurodegeneration and alterations in NVU metabolic coupling or BBB breakdown. In this review we discuss understandings on mitochondria-driven NVU and BBB dysfunction, and how it might be studied in current and prospective NVU/BBB in vitro models for finding new approaches for the efficient pharmacotherapy of Alzheimer’s disease.

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“…Animal studies have considered how these two ‘hits’—early life stress and current life stress—interact to impact outcomes (Calcia et al., 2016; Cao et al., 2021). The combination of early and current life stress may sensitise the central nervous system (CNS) to increases in peripheral inflammation by increasing the permeability of the blood‐brain‐barrier (BBB), allowing peripheral proinflammatory cytokines to infiltrate the CNS (Kuvacheva et al., 2016; Menard et al., 2017), triggering cytokine production within the brain (Bilbo & Schwarz, 2012). Cytokines in the brain have been linked to depression‐like behaviours in animal models, both when cytokines have been administered directly into the brain (Anforth et al., 1998; Dantzer & Kelley, 2007) and when they have infiltrated the brain via a compromised BBB (Menard et al., 2017).…”

Section: Introductionmentioning

confidence: 99%

Depressed, stressed, and inflamed: C‐reactive protein linked with depression symptoms in midlife women with both childhood and current life stress

Metcalf,

Johnson,

Duffy

et al. 2023

Stress and Health

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To determine whether the relationship between inflammatory factors and clinically significant depression symptoms is moderated by high exposure to adverse childhood experiences and current life stressors in a longitudinal community cohort of midlife women. Methods: Participants from the Penn Ovarian Ageing Study community cohort (age at baseline: M = 45.3 [SD = 3.8]) were included in analyses if they had a blood sample measuring basal inflammatory markers during at least one visit where depression symptom severity and current stressful life events were also assessed (N = 142, average number of visits per participant = 1.75 [SD = 0.92]). Approximately annually over the course of 16 years, participants self‐reported depression symptom severity using the Centre for Epidemiologic Studies Depression (CESD) Scale, provided menstrual diaries to determine menopause stage, and contributed blood samples. Residual blood samples were assayed for interleukin (IL)‐6, IL 1‐beta (IL‐1β), tumour necrosis factor alpha (TNF‐α), and high sensitivity C‐reactive protein (hsCRP). Early life stress was quantified using the Adverse Childhood Experiences questionnaire (low [0–1 experience(s)] versus high [≥ 2 experiences]). Current stressful life events were assessed using a structured interview (low [0–1 events] vs. high [≥ 2 events]). Generalised estimating equation models were used to model associations with the outcome of interest—clinically significant depression symptoms (CESD ≥16)—and risk factors: inflammatory marker levels (log transformed), adverse childhood experiences group, and current life stressors group. Covariates included menopause stage, age at study baseline, body mass index, race, and smoking status. We found a significant three‐way interaction between log hsCRP levels, adverse childhood experiences group, and current life stressors group on likelihood of experiencing clinically significant depression symptoms (OR: 4.33; 95% CI: 1.22, 15.46; p = 0.024) after adjusting for covariates. Solely for women with high adverse childhood experiences and with high current life stressors, higher hsCRP was associated with higher odds of having clinically significant depression symptoms (OR: 1.46; 95% CI 1.07, 1.98; p = 0.016). This three‐way interaction was not significant for IL‐6, IL‐1β, or TNF‐α. For women in midlife with exposure to high adverse childhood experiences and multiple current life stressors, elevated levels of CRP were uniquely associated with clinically significant depression symptoms. Early life adversity and current life stressors represent identifiable individual risk factors whose negative impact may be curtailed with inventions to target inflammation in midlife women.

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Tight junction proteins of cerebral endothelial cells in early postnatal development

Cited by 9 publications

References 20 publications

Early life stress sensitizes individuals to the psychological correlates of mild fluctuations in inflammation

Early life stress sensitizes individuals to the psychological correlates of mild fluctuations in inflammation

Blood–Brain Barrier and Neurovascular Unit In Vitro Models for Studying Mitochondria-Driven Molecular Mechanisms of Neurodegeneration

Depressed, stressed, and inflamed: C‐reactive protein linked with depression symptoms in midlife women with both childhood and current life stress

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