Introduction to Brain Microvessel

What is/are Brain Microvessel?

Brain Microvessel - 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. ^[1] Methods We evaluated the thickness of the basement membrane and the length of brain microvessels, by immunohistochemistry, in AβPPswe/PS1A246E (AD) transgenic mice and non-transgenic mice (NT) bearing one (TTR+/−) or two (TTR+/+) copies of the TTR gene. ^[2] Here, to understand the spatial distribution and the potential sequestration of parasites in the whole-brain microvessels during a mouse model of ECM, we utilized the new tissue-clearing method CUBIC (Clear, Unobstructed, Brain/Body Imaging Cocktails and Computational analysis) with light sheet fluorescent microscopy (LSFM), and reconstructed images in three-dimensions (3D). ^[3] Moreover, increased expression of matrix metalloproteinase-3 (MMP-3) and MMP-9 and decreased expression of tight junction proteins, zonula occludens-1 (ZO-1) and occludin, were observed in brain microvessels of CIA rats. ^[4] The protection was associated with the inability of brain microvessels from Cd74−/− hosts to present parasite antigen to sequestered Plasmodium-specific CD8+ T cells. ^[5] This study was aimed to characterize structural alterations and potential mechanisms in brain microvessels before and after ischemic stroke in type 2 diabetic rats treated with high-fat diet and streptozotocin (HFD/STZ). ^[6] Then findings of diverse immunoreactivity for P2X1, P2X2, P2X4, and P2X6 receptors associated with brain microvessels are shown, including vascular endothelium and pericytes as well as perivascular astrocytes and neuronal components. ^[7] Such optical attenuation reduces the achievable spatial resolution and precludes the visualization of small features such as brain microvessels. ^[8] Our results showed an impairment in post-stroke vascular remodeling under T2DM condition, reflected by the decreased expression of trophic factors in brain microvessels and impairments of angiogenesis. ^[9] In our approach, brain microvessels, which retain their endfoot processes, were isolated from mouse brain and dissociated, whereupon endfeet were recovered using an antibody-based column astrocyte isolation kit. ^[10] The cytotoxicity of PEG-PBCA to brain microvessel endothelial cells (BMVEC) decreases with the extension of the PEG chain and the shortening of the PBCA chain. ^[11] Brain microvessel and endothelia were isolated for RNA sequencing to explore the molecular pathway. ^[12] Although retinal microvessels (RMVs) and brain microvessels (BMVs) are closely related in their developmental and share similar blood-neural barriers, studies have reported markedly different responses to stressors such as diabetes. ^[13] AD transgenic mice with TTR genetic reduction, AD/TTR+/−, exhibited a thicker BM in brain microvessels and decreased vessel length than animals with normal TTR levels, AD/TTR+/+. ^[14] ABSTRACT The negative surface charge of brain microvessel endothelial cells is derived from the special composition of their membrane lipids and the thick endothelial surface glycocalyx. ^[15] Delivery of putative compounds of therapeutic value to the brain is limited by brain barriers: the blood–brain barrier located in the endothelium of the brain microvessels (BrMV) and the blood–cerebrospinal fluid barrier located in the epithelium of the choroid plexus (ChP). ^[16] Sex is an important determinant of brain microvessels (MVs) function and susceptibility to cerebrovascular and neurological diseases, but underlying mechanisms are unclear. ^[17] To overcome this problem, we carried out four-dimensional (x–y–z–t) imaging of brain microvessels during exposure to vasoactive molecules in order to constrain the impact of brain movements on the recordings. ^[18] Breast cancer resistance protein (BCRP) is one of ATP-binding cassette (ABC) transporters in brain microvessel endothelial cells that transport their substrates from brain to blood, thus limiting substrates to crossing into brain through blood–brain barrier. ^[19] Importantly, impaired endothelial β-catenin signaling abrogated the expression of the VEGFR (vascular endothelial growth factor receptor)-2 and VEGFR3 in brain microvessels but not in the lung endothelium. ^[20] Gene analysis in brain microvessels of DM type 2 db/db animals showed alterations of similar genes as in DM 1 model, some to an even greater extent. ^[21] To explore whether OPCs may actually be recruited within the neurovascular unit (NVU), de facto intervening in its cellular and molecular composition, we quantified by immunoconfocal morphometry the presence of OPCs in contact with brain microvessels, during postnatal cerebral cortex vascularization at postnatal day 6, in wild-type (WT) and NG2 knock-out (NG2KO) mice, and in the cortex of adult naïve and EAE-affected WT and NG2KO mice. ^[22] Taken together, our results indicate that GPR55 activation modulates the function of endothelial cells of brain microvessels, produces a transient reduction in endothelial barrier function and increases BBB permeability. ^[23] The mutant IDH1 knock-in also impeded the pericyte coverage of brain microvessels in mice. ^[24] Investigation on brain microvessel protein expressions using two-dimensional (2D) gel electrophoresis coupled with LC-MS/MS showed that proteins involved in mitochondrial energy metabolism, transcription regulation, cytoskeleton maintenance and signaling pathways were differently expressed. ^[25] This optical attenuation reduces the achievable spatial resolution, precluding the visualization of small features such as brain microvessels. ^[26] 5-conjugated dextran in brain microvessels) with adaptive optics to compensate for tissue-induced aberrations in the wavefront. ^[27] Sequestration of Plasmodium-infected red blood cells (iRBCs) in brain microvessels is a hallmark of CM pathology. ^[28] Our study, therefore, demonstrates that brain microvessels are vulnerable to a high PP and mechanical stress associated with transverse aortic constriction, promoting severe vascular dysfunction, disruption of the neurovascular unit, and cognitive decline. ^[29] Swiss outbred mice received an 11-day treatment of CQ (30 mg/kg) by oral gavage, after which brain microvessel-enriched fractions (MEFs) and surrounding interfaces (subcortical brain tissue and plasma) were extracted. ^[30] NEW METHOD Efficient isolation of brain microvessels requires the elimination of meninges, vessels of high caliber vessels and choroid plexus, commonly done by rolling the over filter paper, but can't be done on other CNS regions. ^[31] At the same time, lead content in blood, cerebrospinal fluid,choroid plexus, brain microvessels and bones increased. ^[32] Dried grape products are also applied in Iranian traditional medicine for memory problems, which are linked to the pathology of brain microvessels, a special part of the cardiovascular system. ^[33] To elucidate the metabolic dynamics of Aβ surrounding the brain microvessels, we identified Aβ-degrading activity in human serum (blood Aβ-degrading activity: BADA) by column chromatography and LC/MS. ^[34] Highlights Alkaline phosphatase activity in brain microvessels is diminished in sepsis. ^[35] Brain microvessels were isolated to further evaluate vascular alterations after amphetamine exposure. ^[36] The BBB is a selectively permeable barrier characterized by brain microvessels which are composed of endothelial cells mortared by tight-junction proteins. ^[37] The extrahepatic CYP enzymes, CYP1B1 and CYP2U1, have been predominantly found in both astrocytes and brain microvessels. ^[38]

blood brain barrier

Background: The in vivo restrictive properties of the blood brain barrier (BBB) largely arise from astrocyte and pericyte synergistic cell signaling interactions that underlie the brain microvessel endothelial cells (BMEC). ^[1] The blood-brain barrier (BBB) is a highly selective membrane barrier at the brain microvessel level that facilitates transport between the systemic circulation and the central nervous system. ^[2] Background Brain microvessel endothelial cells constitute an important component in the blood-brain barrier. ^[3] The effect of cannabidiol (CBD), a high-affinity agonist of the transient receptor potential vanilloid-2 (TRPV2) channel, has been poorly investigated in human brain microvessel endothelial cells (BMEC) forming the blood-brain barrier (BBB). ^[4] The brain is isolated from the whole body by the blood-brain barrier (BBB) which is located in brain microvessel endothelial cells (ECs). ^[5]

Human Brain Microvessel

Our results showed that circ_CHFR and EGFR expressions were dramatically upregulated, while miR-15a-5p expression was downregulated in ox-LDL-induced human brain microvessel endothelial cells (HBMECs) relative to control groups. ^[1] In cultured human brain microvessel endothelial cells (hBMVECs), thrombin induced F-actin stress fiber formation causes barrier disruption via activating eNOS. ^[2] In vitro uptake studies with human brain microvessel endothelial cells (hCMEC/D3 cells) showed preferential uptake of muscle-type CK (CK-MM) compared with brain-type CK (CK-BB) at the BBB. ^[3] Methods The conditioned media from LBH regulated human glioma cell lines and patient-derived glioma stem cells (GSCs) were used to treat the human brain microvessel endothelial cells (hBMECs). ^[4] The effect of cannabidiol (CBD), a high-affinity agonist of the transient receptor potential vanilloid-2 (TRPV2) channel, has been poorly investigated in human brain microvessel endothelial cells (BMEC) forming the blood-brain barrier (BBB). ^[5] The ΔatlASS strain also attenuated bacterial adherence in human brain microvessel endothelial cells (HBMECs). ^[6] The aim of this study was to investigate the role of miR-25-5p in oxidized low-density lipoprotein (ox-LDL)-treated human brain microvessel endothelial cells (HBMECs) and the underlying mechanisms. ^[7] Human brain microvessel ECs were transfected with miR‐125a‐5p mimic or miR‐125a‐5p short hairpin RNA to obtain miR‐125a‐5p overexpressing ECs and miR‐125a‐5p knockdown ECs, and their derived EMVs. ^[8] Here, we have developed an engineered 3D human brain microvessel model that mimics the blood flow rates and architecture of small blood vessels to study how P. ^[9]

Mouse Brain Microvessel

The protein and mRNA levels of zonula occludens-1 (ZO-1), occludin, NEP, receptor for advanced glycation end products (RAGE), and low-density lipoprotein receptor-related protein 1 (LRP1) in mouse brain microvessels were, respectively, analyzed by Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) analyses. ^[1] We confirmed that knocking down of Khdrbs2 or Hey2 increased the expression levels of ZO-1, occludin, and claudin-5 in APP/PS1 mice brain microvessels. ^[2] Furthermore, the expression of p-ERM and p-MLC in hCMEC/D3 as well as mice brain microvessels were significantly upregulated, but no significant change on the expression of TJs proteins (ZO-1, Occludin and Claudin-3). ^[3] In order to shed light on the events taking place at the NVU in brain diseases, we performed next generation sequencing, employing the MACE technology, of mouse brain microvessels (MBMVs) from an Alzheimer’s disease (AD) mouse model, harbouring the Thy1-SwDI triple mutation of amyloid precursor protein (APP), and compared it to aged-matched WT mice at 6 and 18 month-of-age. ^[4] We found that the expression of FBW7 was decreased in mouse brain microvessels from high-fat diet (HFD)-fed atherosclerotic mice. ^[5]

Rat Brain Microvessel

In addition, primary rat brain microvessel endothelial cells (rBMECs) with oxygen glucose deprivation (OGD) were applied to further verify the possible mechanisms of Cur20-induced angiogenesis. ^[1] Material/Methods Rat brain microvessel endothelial cells (BMECs) were cultured in 10% FBS and 1% penicillin/streptomycin. ^[2] To provide proof of concept and initial validation data, Ag-NPs and Au-NPs were tested in 3 different cell cultures including rat brain microvessel endothelial cells, mouse neural stem cells, and the human SH-SY5Y cell line. ^[3]

Isolated Brain Microvessel

Genic expression of ABC transporters, including P-gp, BCRP, MRP1, MRP2, MRP4 and MRP5 was evaluated by RT-qPCR on isolated brain microvessels. ^[1] However, a different CCL2 temporal profile was observed in whole brain homogenate, cerebrospinal fluid, and isolated brain microvessels, with a progressive increase over 24 hours, demonstrating a mismatch between brain versus plasma responses. ^[2] HIR notably increased plasma arginase activity and lowered Arg level, increased the BBB permeability accompanied with enhanced brain water, and decreased the proliferative cells (marked by Ki67) in cerebral microvessels (marked by CD31) and protein expressions of cyclin A, cyclin D, CDK2 and CDK4 in isolated brain microvessels. ^[3]

Primary Brain Microvessel

Furthermore, artemisinin restored LPS‐induced decrease of junction proteins ZO‐1, Occludin and Claudin‐5 in primary brain microvessel endothelial cells, and attenuated LPS‐induced blood–brain barrier disruption in mice as assessed by Evans blue. ^[1] Similarly, cultures of primary brain microvessel endothelial cells from middle‐aged female rats and exposed to stroke‐like conditions (oxygen glucose deprivation; OGD) confirmed that IGF‐1 reduced dye transfer across this cell monolayer. ^[2]

brain microvessel endothelial

Background: The in vivo restrictive properties of the blood brain barrier (BBB) largely arise from astrocyte and pericyte synergistic cell signaling interactions that underlie the brain microvessel endothelial cells (BMEC). ^[1] 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. ^[2] Our results showed that circ_CHFR and EGFR expressions were dramatically upregulated, while miR-15a-5p expression was downregulated in ox-LDL-induced human brain microvessel endothelial cells (HBMECs) relative to control groups. ^[3] Furthermore, artemisinin restored LPS‐induced decrease of junction proteins ZO‐1, Occludin and Claudin‐5 in primary brain microvessel endothelial cells, and attenuated LPS‐induced blood–brain barrier disruption in mice as assessed by Evans blue. ^[4] In addition, primary rat brain microvessel endothelial cells (rBMECs) with oxygen glucose deprivation (OGD) were applied to further verify the possible mechanisms of Cur20-induced angiogenesis. ^[5] The cytotoxicity of PEG-PBCA to brain microvessel endothelial cells (BMVEC) decreases with the extension of the PEG chain and the shortening of the PBCA chain. ^[6] ABSTRACT The negative surface charge of brain microvessel endothelial cells is derived from the special composition of their membrane lipids and the thick endothelial surface glycocalyx. ^[7] Breast cancer resistance protein (BCRP) is one of ATP-binding cassette (ABC) transporters in brain microvessel endothelial cells that transport their substrates from brain to blood, thus limiting substrates to crossing into brain through blood–brain barrier. ^[8] Background Brain microvessel endothelial cells constitute an important component in the blood-brain barrier. ^[9] In cultured human brain microvessel endothelial cells (hBMVECs), thrombin induced F-actin stress fiber formation causes barrier disruption via activating eNOS. ^[10] In vitro uptake studies with human brain microvessel endothelial cells (hCMEC/D3 cells) showed preferential uptake of muscle-type CK (CK-MM) compared with brain-type CK (CK-BB) at the BBB. ^[11] Methods The conditioned media from LBH regulated human glioma cell lines and patient-derived glioma stem cells (GSCs) were used to treat the human brain microvessel endothelial cells (hBMECs). ^[12] The effect of cannabidiol (CBD), a high-affinity agonist of the transient receptor potential vanilloid-2 (TRPV2) channel, has been poorly investigated in human brain microvessel endothelial cells (BMEC) forming the blood-brain barrier (BBB). ^[13] The ΔatlASS strain also attenuated bacterial adherence in human brain microvessel endothelial cells (HBMECs). ^[14] The brain is isolated from the whole body by the blood-brain barrier (BBB) which is located in brain microvessel endothelial cells (ECs). ^[15] The aim of this study was to investigate the role of miR-25-5p in oxidized low-density lipoprotein (ox-LDL)-treated human brain microvessel endothelial cells (HBMECs) and the underlying mechanisms. ^[16] Similarly, cultures of primary brain microvessel endothelial cells from middle‐aged female rats and exposed to stroke‐like conditions (oxygen glucose deprivation; OGD) confirmed that IGF‐1 reduced dye transfer across this cell monolayer. ^[17] Material/Methods Rat brain microvessel endothelial cells (BMECs) were cultured in 10% FBS and 1% penicillin/streptomycin. ^[18] To provide proof of concept and initial validation data, Ag-NPs and Au-NPs were tested in 3 different cell cultures including rat brain microvessel endothelial cells, mouse neural stem cells, and the human SH-SY5Y cell line. ^[19]