Chloride intracellular channel 4 is required for maturation of the cerebral collateral circulation

Lucitti, Jennifer L.; Tarte, Natalie J.; Faber, James E.

doi:10.1152/ajpheart.00451.2015

Cited by 15 publications

(12 citation statements)

References 47 publications

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“…No additional decrease occurred at 18 months of age (~ 56 hye). Absence of effect at 1 month indicates that the presence of fewer and smaller collaterals is not due to decreased collaterogenesis, which occurs in the perinatal period and determines collateral number and diameter in the adult [ 25 – 28 ]. The latter could possibly have occurred secondary to parenchymal Aβ that has been detected in 1-month-old transgenic AD mice [ 45 ], or from non-specific effects of transgene insertion or private mutations/genetic drift in the AD strains.…”

Section: Resultsmentioning

confidence: 99%

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Mouse models of Alzheimer’s disease cause rarefaction of pial collaterals and increased severity of ischemic stroke

2018

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Vascular dysfunction contributes to the progression and severity of Alzheimer’s disease (AD). Patients with AD also sustain larger infarctions after ischemic stroke; however, the responsible mechanisms are unknown. Pial collaterals are the primary source of protection in stroke. Unfortunately, natural aging and other vascular risk factors cause a decline in collateral number and diameter (rarefaction) and an increase in stroke severity. Herein, we tested the hypothesis that AD accelerates age-induced collateral rarefaction and examined potential underlying mechanisms. Triple and double transgenic mouse models of AD both sustained collateral rarefaction by 8 months of age, well before the onset of rarefaction caused by aging alone (16 months of age). Rarefaction, which did not progress further at 18 months of age, was accompanied by a twofold increase in infarct volume after MCA occlusion. AD did not induce rarefaction of similarly sized pial arterioles or penetrating arterioles. Rarefaction was minimal and occurred only at 18 months of age in a parenchymal vascular amyloid-beta model of AD. Rarefaction was not associated with amyloid-beta deposition on collaterals or pial arteries, nor was plaque burden or CD11b + cell density greater in brain underlying the collateral zones versus elsewhere. However, rarefaction was accompanied by increased markers of oxidative stress, inflammation, and aging of collateral endothelial and mural cells. Moreover, rarefaction was lessened by deletion of CX 3 CR1 and prevented by overexpression of eNOS. These findings demonstrate that mouse models of AD promote rarefaction of pial collaterals and implicate inflammation-induced accelerated aging of collateral wall cells. Strategies that reduce vascular inflammation and/or increase nitric oxide may preserve collateral function. Electronic supplementary material The online version of this article (10.1007/s10456-018-9655-0) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

“…Unfortunately, collateral extent varies widely among individuals. In mice, pial collaterals form late during gestation and undergo perinatal maturation that determines their extent in the adult [ 25 – 28 ]. This collaterogenesis process varies widely due to differences in genetic background [ 23 , 24 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

Mouse models of Alzheimer’s disease cause rarefaction of pial collaterals and increased severity of ischemic stroke

2018

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“…Clic4 gene deficiency results in reduced expression of Vegfr2 , Vegfr1 , Vegfc , and mural cell markers associated with a reduction in ischemia-induced expression of hypoxia inducible factor-1α (HIF-1α)5). Recent work showed that overexpression of VEGF-A in Clic4 (-/-) mice rescued defects in collateral maturation by preventing mural cell loss and collateral pruning, thus restoring collateral number and diameter and reducing stroke severity in adults23). In fact, hCMEC/D3 showed high Clic4 mRNA and protein expression, whereas HUVEC did not (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Proteomic Analysis of a Rat Cerebral Ischemic Injury Model after Human Cerebral Endothelial Cell Transplantation

Choi

Yun

Lee

et al. 2016

J Korean Neurosurg Soc

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ObjectiveCerebral endothelial cells have unique biological features and are fascinating candidate cells for stroke therapy.MethodsIn order to understand the molecular mechanisms of human cerebral endothelial cell (hCMEC/D3) transplantation in a rat stroke model, we performed proteomic analysis using 2-dimensional electrophoresis and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Protein expression was confirmed by quantitative real-time PCR and Western blot.ResultsSeveral protein spots were identified by gel electrophoresis in the sham, cerebral ischemia (CI), and CI with hCMEC/D3 treatment cerebral ischemia with cell transplantation (CT) groups, and we identified 14 differentially expressed proteins in the CT group. Proteins involved in mitochondrial dysfunction (paraplegin matrix AAA peptidase subunit, SPG7), neuroinflammation (peroxiredoxin 6, PRDX6), and neuronal death (zinc finger protein 90, ZFP90) were markedly reduced in the CT group compared with the CI group. The expression of chloride intracellular channel 4 proteins involved in post-ischemic vasculogenesis was significantly decreased in the CI group but comparable to sham in the CT group.ConclusionThese results contribute to our understanding of the early phase processes that follow cerebral endothelial cell treatment in CI. Moreover, some of the identified proteins may present promising new targets for stroke therapy.

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“…CLIC4 plays a role in the acidification of intracellular vacuoles that are required for tubulogenesis (Ulmasov et al, 2009). Clic4 -/mice exhibit aberrant collateral circulation in response to ischemic injury (Chalothorn, Zhang, Smith, Edwards, & Faber, 2009;Lucitti, Tarte, & Faber, 2015).…”

Section: Clic4mentioning

confidence: 99%

Three Decades of Chloride Intracellular Channel Proteins: From Organelle to Organ Physiology

et al. 2018

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Intracellular organelles are membranous structures central for maintaining cellular physiology and the overall health of the cell. To maintain cellular function, intracellular organelles are required to tightly regulate their ionic homeostasis. Any imbalance in ionic concentrations can disrupt energy production (mitochondria), protein degradation (lysosomes), DNA replication (nucleus), or cellular signaling (endoplasmic reticulum). Ionic homeostasis is also important for volume regulation of intracellular organelles and is maintained by cation and anion channels as well as transporters. One of the major classes of ion channels predominantly localized to intracellular membranes is chloride intracellular channel proteins (CLICs). They are non-canonical ion channels with six homologs in mammals, existing as either soluble or integral membrane protein forms, with dual functions as enzymes and channels. Provided in this overview is a brief introduction to CLICs, and a summary of recent information on their localization, biophysical properties, and physiological roles. © 2018 by John Wiley & Sons, Inc.

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Chloride intracellular channel 4 is required for maturation of the cerebral collateral circulation

Abstract: Lucitti JL, Tarte NJ, Faber JE. Chloride intracellular channel 4 is required for maturation of the cerebral collateral circulation.

Cited by 15 publications

References 47 publications

Mouse models of Alzheimer’s disease cause rarefaction of pial collaterals and increased severity of ischemic stroke

Mouse models of Alzheimer’s disease cause rarefaction of pial collaterals and increased severity of ischemic stroke

Proteomic Analysis of a Rat Cerebral Ischemic Injury Model after Human Cerebral Endothelial Cell Transplantation

Three Decades of Chloride Intracellular Channel Proteins: From Organelle to Organ Physiology

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