cAMP-Mediated regulation of the permeability in the brain capillaries

1975 ◽  
Vol 31 (5) ◽  
pp. 582-584 ◽  
Author(s):  
F. Joó ◽  
Z. Rakonczay ◽  
M. Wollemann
Keyword(s):  
Brain Capillaries ◽  
The Brain

scholarly journals Endothelial cell-specific reduction of heparan sulfate suppresses glioma growth in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Takamasa Kinoshita ◽  
Hiroyuki Tomita ◽  
Hideshi Okada ◽  
Ayumi Niwa ◽  
Fuminori Hyodo ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Heparan Sulfate ◽  
Vascular Endothelium ◽  
Wild Type ◽  
Brain Capillaries ◽  
Gene Encoding ◽  
Glioma Growth ◽  
Underlying Mechanisms ◽  
The Brain

Abstract Purpose Heparan sulfate (HS) is one of the factors that has been suggested to be associated with angiogenesis and invasion of glioblastoma (GBM), an aggressive and fast-growing brain tumor. However, it remains unclear how HS of endothelial cells is involved in angiogenesis in glioblastoma and its prognosis. Thus, we investigated the effect of endothelial cell HS on GBM development. Methods We generated endothelial cell-specific knockout of Ext1, a gene encoding a glycosyltransferase and essential for HS synthesis, and murine GL261 glioblastoma cells were orthotopically transplanted. Two weeks after transplantation, we examined the tumor progression and underlying mechanisms. Results The endothelial cell-specific Ext1 knockout (Ext1CKO) mice exhibited reduced HS expression specifically in the vascular endothelium of the brain capillaries compared with the control wild-type (WT) mice. GBM growth was significantly suppressed in Ext1CKO mice compared with that in WT mice. After GBM transplantation, the survival rate was significantly higher in Ext1CKO mice than in WT mice. We investigated how the effect of fibroblast growth factor 2 (FGF2), which is known as an angiogenesis-promoting factor, differs between Ext1CKO and WT mice by using an in vivo Matrigel assay and demonstrated that endothelial cell-specific HS reduction attenuated the effect of FGF2 on angiogenesis. Conclusions HS reduction in the vascular endothelium of the brain suppressed GBM growth and neovascularization in mice.

Mural Cells in the Brain Capillaries: Pericytes

2021 ◽  
Author(s):  
Ruihua Sun ◽  
Wei Li ◽  
Chenhao Gao ◽  
Jiewen Zhang ◽  
Junkui Shang
Keyword(s):  
Brain Capillaries ◽  
Mural Cells ◽  
The Brain

Iron uptake in relation to transferrin degradation in brain and other tissues of rats

1992 ◽  
Vol 263 (4) ◽  
pp. R924-R929 ◽  
Author(s):  
M. E. Strahan ◽  
A. Crowe ◽  
E. H. Morgan
Keyword(s):  
Iron Uptake ◽  
Brain Capillaries ◽  
Total Rate ◽  
The Brain ◽  
Rat Reticulocytes ◽  
Rate Of Accumulation

The possibility that iron uptake by the brain involves transcytosis of the iron-transferrin complex across the brain capillaries, followed by degradation of the transferrin (Tf) within the brain, was investigated using diferric 125I-[59Fe]Tf and [59Fe]Tf coupled to 125I-tyramine cellobiose (TC). The radiolabeled catabolic products of proteins labeled with 125I-TC remain in the cells where degradation occurs. The TCTf complex behaved normally with respect to its ability to donate iron to rat reticulocytes in vitro or to the brain, liver, kidneys, and femurs in vivo. In the brain there was little difference in the uptake of 125I derived from Tf and TCTf, and the amounts were equivalent to only a small fraction of the 59Fe uptake. Hence, the rate of Tf catabolism in the brain was insufficient to account for the rate of accumulation of iron from plasma Tf. It was concluded that Tf recycles to the plasma after delivering its iron to the brain. The uptake of 125I from TCTf by the liver and kidneys accounted for 40-50% of the total rate of Tf catabolism. This indicated that they were important but not the only sites of degradation of this protein.

scholarly journals Amyloid β oligomers constrict human capillaries in Alzheimer’s disease via signaling to pericytes

Science ◽  
2019 ◽  
Vol 365 (6450) ◽  
pp. eaav9518 ◽  
Author(s):  
Ross Nortley ◽  
Nils Korte ◽  
Pablo Izquierdo ◽  
Chanawee Hirunpattarasilp ◽  
Anusha Mishra ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Reactive Oxygen Species ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Oxygen Species ◽  
Brain Capillaries ◽  
Disease Relevance ◽  
The Brain ◽  
Capillary Walls

Cerebral blood flow is reduced early in the onset of Alzheimer’s disease (AD). Because most of the vascular resistance within the brain is in capillaries, this could reflect dysfunction of contractile pericytes on capillary walls. We used live and rapidly fixed biopsied human tissue to establish disease relevance, and rodent experiments to define mechanism. We found that in humans with cognitive decline, amyloid β (Aβ) constricts brain capillaries at pericyte locations. This was caused by Aβ generating reactive oxygen species, which evoked the release of endothelin-1 (ET) that activated pericyte ETA receptors. Capillary, but not arteriole, constriction also occurred in vivo in a mouse model of AD. Thus, inhibiting the capillary constriction caused by Aβ could potentially reduce energy lack and neurodegeneration in AD.

Screen filtration pressure of homologous and heterologous blood and electroencephalogram

1964 ◽  
Vol 206 (4) ◽  
pp. 811-814 ◽  
Author(s):  
Hans Hirsch ◽  
Roy L. Swank ◽  
Marianne Breuer ◽  
Wolfgang Hissen
Keyword(s):  
Blood Flow ◽  
Electrical Activity ◽  
Blood Cells ◽  
Perfusion Pressure ◽  
Glass Wool ◽  
Brain Capillaries ◽  
Perfusion Rate ◽  
Brain Waves ◽  
Filtration Pressure ◽  
The Brain

The character and duration of electrical activity arising from a completely isolated cat's head was dependent upon the screen filtration pressure (SFP) of the heparinized oxygenated blood with which it was perfused. If the SFP was above normal the amplitude and frequency of the EEG first decreased, then the brain waves disappeared. The duration of time from the beginning of perfusion until these changes in the EEG occurred was inversely related to the SFP of the perfused blood. Also, the perfusion rate was inversely related to the SFP provided the perfusion pressure remained the same. It is believed that the increase in SFP and changes in EEG and blood flow were due to the presence in the blood of aggregates of blood cells (platelets and leucocytes) which obstructed the brain capillaries. It would appear that heterologous (dog) as well as homologous (cat) blood can be effectively used to perfuse the isolated cat's head provided the blood has a normal SFP. In practice, this was made possible by filtering the blood continuously through Pyrex glass wool.

Pathogenesis of Brain Edema and Hemorrhage: Role of the Brain Capillary

PEDIATRICS ◽  
1979 ◽  
Vol 64 (3) ◽  
pp. 357-360
Author(s):  
Gary W. Goldstein
Keyword(s):  
Endothelial Cells ◽  
Brain Edema ◽  
Tight Junctions ◽  
Interstitial Fluid ◽  
Water Soluble ◽  
Brain Capillaries ◽  
Reye's Syndrome ◽  
Anatomic Site ◽  
Brain Capillary ◽  
The Brain

It has recently been shown that the endothelial cells in brain capillaries are the anatomic site of the blood-brain barrier, and that these endothelial cells act to maintain a constant composition and volume of brain interstitial fluid.1-3 Defects in brain capillary function appear to play a role in the pathogenesis of brain edema and hemorrhage in a wide variety of diseases. Conditions as diverse as intraventricular hemorrhage of the premature, asphyxia neonatorum, lead poisoning, head injury, Reye's syndrome, osmolar coma, and the brain edema surrounding a tumor or abscess may all share the common feature of brain capillary failure. In this review, I will consider some recent advances in our understanding of the brain microvasculature that may explain their unusual susceptibility to injury. Brain capillaries have a number of important differences from capillaries in other organs. A schematic of a typical brain capillary is shown in the Figure. Unlike systemic capillaries, the endothelial cells in brain capillaries are joined together by tight junctions.3 These cellular junctions are present around the entire circumference of the capillary tube. The result is a continuous layer of endothelial cells that effectively separate the plasma from the interstitial fluid of the brain. The tight junctions are composed of a series of complex interdigitations that create a barrier so complete that water-soluble molecules and ions are unable to move into the brain between the endothelial cells. In other organs, the capillaries do not have tight junctions, and sugars, amino acids, ions, and drugs readily diffuse between endothelial cells into the interstitial fluid.

scholarly journals Regulation of P-glycoprotein expression in brain capillaries in Huntington’s disease and its impact on brain availability of antipsychotic agents risperidone and paliperidone

2015 ◽  
Vol 36 (8) ◽  
pp. 1412-1423 ◽  
Author(s):  
Yu-Han Kao ◽  
Yijuang Chern ◽  
Hui-Ting Yang ◽  
Hui-Mei Chen ◽  
Chun-Jung Lin
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Mrna Level ◽  
Antipsychotic Agents ◽  
Brain Capillaries ◽  
P Glycoprotein ◽  
Exogenous Expression ◽  
And Function ◽  
The Brain ◽  
Polyq Tract

Huntington’s disease (HD) is a neurodegenerative disease marked by an expanded polyglutamine (polyQ) tract on the huntingtin (HTT) protein that may cause transcriptional dysfunction. This study aimed to investigate the regulation and function of P-glycoprotein, an important efflux transporter, in brain capillaries in HD. The results showed that, compared with the littermate controls, R6/2 HD transgenic mice with the human mutant HTT gene had higher levels of P-glycoprotein mRNA and protein and enhanced NF-κB activity in their brain capillaries. Higher P-glycoprotein expression was also observed in the brain capillaries of human HD patients. Consistent with this enhanced P-glycoprotein expression, brain extracellular levels and brain-to-plasma ratios of the antipsychotic agents risperidone and paliperidone were significantly lower in R6/2 mice than in their littermate controls. Exogenous expression of human mutant HTT protein with expanded polyQ (mHTT-109Q) in HEK293T cells enhanced the levels of P-glycoprotein transcripts and NF-κB activity compared with cells expressing normal HTT-25Q. Treatment with the IKK inhibitor, BMS-345541, decreased P-glycoprotein mRNA level in cells transfected with mHTT-109Q or normal HTT-25Q. In conclusion, mutant HTT altered the expression of P-glycoprotein through the NF-κB pathway in brain capillaries in HD and markedly affected the availability of P-glycoprotein substrates in the brain.

Filtration Coefficient of the Capillaries of the Brain

1958 ◽  
Vol 195 (2) ◽  
pp. 459-464 ◽  
Author(s):  
N. A. Coulter
Keyword(s):  
Filtration Rate ◽  
Filtration Coefficient ◽  
Secretory Process ◽  
Brain Capillaries ◽  
Brain Capillary ◽  
Average Value ◽  
Capillary Membranes ◽  
The Brain ◽  
Muscle Capillaries

The Monro-Kellie doctrine was used as the basis for determination of the filtration coefficient of the capillaries of the cat's brain. An average value of 10.3 x 10–8 ml/sec/cm H2O/cm2 was found. A linear relation was observed between filtration rate and filtration pressure. The fact that the filtration coefficient of brain capillaries is somewhat higher than that of muscle capillaries suggests that lipoid insoluble molecules actually penetrate the brain capillary membranes readily, but are pumped back by a secretory process.

Changes in the glucose transporter of brain capillaries

1992 ◽  
Vol 70 (S1) ◽  
pp. S113-S117 ◽  
Author(s):  
Sami I. Harik
Keyword(s):  
Alzheimer Disease ◽  
Blood Brain Barrier ◽  
Glucose Transporter ◽  
Glucose Transporters ◽  
Brain Barrier ◽  
Capillary Endothelium ◽  
Brain Capillaries ◽  
Glut 1 ◽  
Blood Brain ◽  
The Brain

Brain capillary endothelium has a high density of the GLUT-1 facilitative glucose transporter protein. This is reasonable in view of the brain's high metabolic rate for glucose and its isolation behind unique capillaries with blood – brain barrier properties. Thus, the brain endothelium, which constitutes less than 0.1% of the brain weight, has to transport glucose for the much larger mass of surrounding neurons and glia. I describe here the changes that occur in the density of glucose transporters in brain capillaries of subjects with Alzheimer disease, where there is a decreased cerebral metabolic rate for glucose, and in a novel clinical entity characterized by defective glucose transport at the blood – brain barrier. In subjects with Alzheimer disease, cerebral microvessels showed a marked decrease in the density of the glucose transporter when compared with age-matched controls, but there was no change in the density of glucose transporters in erythrocyte membranes. Thus, I believe that the decreased density of glucose transporters in the brains of subjects with Alzheimer disease is the result rather than the cause of the disease. In contradistinction, the primary defect in glucose transport at the blood – brain barrier in subjects with the recently described entity is associated with decreased density of GLUT-1 in erythrocyte membranes.Key words: brain microvessels, capillary endothelium, blood – brain barrier, glucose transporter, Alzheimer disease, hypoglycorrhachia.

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