Microvascular pericytes in brain-associated vascular disease

Liu, Qi; Yang, Yingxi; Fan, Xiao-Nong

doi:10.1016/j.biopha.2019.109633

Cited by 28 publications

(32 citation statements)

References 139 publications

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“…Indeed, PCs are required for an appropriate brain vascularization at the embryonic stage, predominantly by stabilizing the new vessels' formation [132] and, during the early postnatal stage, by inducing BBB functional properties [133]. Their functional role is played in cooperation with the nearby cells thus being pivotal in the neurovascular unit (NVU), an assorted structure composed of different cell types, including PCs, extracellular matrix proteins setting up the basal lamina, astrocytes, microglia and neurons [134].…”

Section: Cadmium and Pericytesmentioning

confidence: 99%

Cadmium-Induced Oxidative Stress: Focus on the Central Nervous System

et al. 2020

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Cadmium (Cd), a category I human carcinogen, is a well-known widespread environmental pollutant. Chronic Cd exposure affects different organs and tissues, such as the central nervous system (CNS), and its deleterious effects can be linked to indirect reactive oxygen species (ROS) generation. Since Cd is predominantly present in +2 oxidation state, it can interplay with a plethora of channels and transporters in the cell membrane surface in order to enter the cells. Mitochondrial dysfunction, ROS production, glutathione depletion and lipid peroxidation are reviewed in order to better characterize the Cd-elicited molecular pathways. Furthermore, Cd effects on different CNS cell types have been highlighted to better elucidate its role in neurodegenerative disorders. Indeed, Cd can increase blood–brain barrier (BBB) permeability and promotes Cd entry that, in turn, stimulates pericytes in maintaining the BBB open. Once inside the CNS, Cd acts on glial cells (astrocytes, microglia, oligodendrocytes) triggering a pro-inflammatory cascade that accounts for the Cd deleterious effects and neurons inducing the destruction of synaptic branches.

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Section: Cadmium and Pericytesmentioning

confidence: 99%

Cadmium-Induced Oxidative Stress: Focus on the Central Nervous System

et al. 2020

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“…The primary underlying initiating cause of CSVD is the derangement of the blood-brain barrier (BBB), this may start some years before the rst symptoms, leads to the small vessel structural changes and perivascular changes (Liu, Yang, & Fan, 2020), the cellular structure of the BBB is mainly composed of brain microvascular endothelial cells (MVECs) (Wardlaw, 2010). Junction protein (zona occludens-1, occludin, and claudin-5) expression is downregulated in human brain MVECs after high phosphorus treatment (Chung et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

A High Serum Phosphate and Calcium-Phosphate Product is Associated With Cerebral Small Vascular Disease in Patients With Stroke; A Real World Study

Wang

Jiang

et al. 2021

SSRN Journal

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Cerebral small vessel disease (CSVD) is a slowly progress disease, often accompanied by stroke, and result in dementia, depression, cognitive impairment, etc. It had already known that calcium and phosphorus metabolism (CPM) disorders were associated with vascular related adverse events. Serum Ca, P, Ca×P are the most commonly used indicators of CPM in clinical. The risk factors of CSVD and the relationship of serum Ca, P, Ca×P and CSVD in stroke patients who do not have CPM disorders are still obscure. We enrolled 488 CSVD patients in a cohort from a consecutive hospital-based stroke registry, and further subgrouped them into lacunes, white matter hyperintensities (WMHs), cerebral microbleeds (CMBs), and matched them to 140 stroke patients without CSVD as controls. CSVD patients had higher levels of serum Ca, P, Ca×P. We developed 2 predictive models and nomograms (incorporating age, hypertension, P or Ca×P, respectively) for CSVD patients. The prediction and calibration power were good. Area under the curve (AUC) was 0.855, 0.851, respectively. P value of Hosmer-Lemeshow goodness of t (H-L) test was 0.689, 0.698, respectively. P and Ca×P were positive correlated with CSVD, with OR 3720.401 (646.665-21404.249), 1.294 (1.222-1.370), respectively. We further validated the models in lacunes, WMHs, and CMBs, and found models were still valid in these 3 subtypes. In summary, a high serum P or Ca×P are associated with an increased risk of CSVD in stroke patients who without CPM disorders.

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“…While no change in cerebrovascular MMP-9 expression levels was identified between E3FAD and E4FAD animals via ELISA, differences in MMP-9 immunoreactivity in the brain endothelia of these animals were apparent via confocal microscopy. This may be attributable to a greater expression of MMP-9 in endothelial cells specifically, as opposed to whole cerebrovasculature, which is comprised of various other cells, receptors, and proteins [357], [358].…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein E isoforms differentially regulate matrix metallopeptidase 9 function in Alzheimer’s disease

Ringland

Schweig

Paris

et al. 2020

Neurobiology of Aging

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Apolipoprotein E (APOE) is a major genetic risk factor for Alzheimer's disease (AD) and has been shown to influence amyloid-β (Aβ) clearance from the brain in an isoform-specific manner. Our prior work showed Aβ transit across the blood-brain-barrier was reduced by apoE4, compared to other apoE isoforms, due to elevated lipoprotein receptor shedding in brain endothelia. Recently, we demonstrated matrix metallopeptidase 9 (MMP-9) induces lipoprotein receptor proteolysis in an apoE isoform-dependent manner, which impacts Aβ elimination from the brain. The current studies interrogated the relationship between apoE and MMP-9 and found apoE dose-dependently reduced MMP-9 activity in a cell-free assay, with apoE4 showing a significantly weaker ability to inhibit MMP-9 function than apoE2 or apoE3. Moreover, these effects may be due to the reduced binding affinity of apoE4 for MMP-9 compared to apoE2 and apoE3 as revealed by kinetic binding studies. Elevated MMP-9 expression and activity was observed in the cerebrovasculature of both human and animal AD brain specimens with an APOE4 genotype. The apoE isoforms also lead to altered levels of MMP-9 secreted from brain endothelia cultures (apoE2

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Microvascular pericytes in brain-associated vascular disease

Cited by 28 publications

References 139 publications

Cadmium-Induced Oxidative Stress: Focus on the Central Nervous System

Cadmium-Induced Oxidative Stress: Focus on the Central Nervous System

A High Serum Phosphate and Calcium-Phosphate Product is Associated With Cerebral Small Vascular Disease in Patients With Stroke; A Real World Study

Apolipoprotein E isoforms differentially regulate matrix metallopeptidase 9 function in Alzheimer’s disease

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