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Related Concept Videos

Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

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Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this...
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Hemorrhagic Stroke ll: Pathophysiology01:29

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A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
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Ischemic Stroke ll: Pathophysiology01:15

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An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
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DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic...
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Multiple sphingolipid abnormalities following cerebral microendothelial hypoxia.

Fernando D Testai1, John P Kilkus, Evgeny Berdyshev

  • 1Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, Illinois, USA.

Journal of Neurochemistry
|July 26, 2014
PubMed
Summary

Hypoxia causes accumulation of dihydro-sphingolipids in brain cells, potentially protecting against stroke. These changes, including increased sphingosine-1-phosphate and glucosylceramide synthase activity, are reversed by reoxygenation.

Keywords:
ceramidecerebral endotheliumdihydroceramidehypoxiasphingolipids

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Area of Science:

  • Cell Biology
  • Neuroscience
  • Biochemistry

Background:

  • Hypoxia inhibits dihydroceramide (DHC) desaturase, leading to DHC accumulation.
  • Sphingolipids play critical roles in cellular function and response to stress.

Purpose of the Study:

  • To investigate sphingolipid alterations in cerebral microendothelial cells under hypoxic conditions.
  • To determine the role of these changes in endothelial barrier function and cell survival.

Main Methods:

  • Metabolic labeling with [3H]-palmitate.
  • High-performance liquid chromatography/tandem mass spectrometry (HPLC/MS/MS) analysis.
  • Use of specific inhibitors (myriocin, GW-4869, EtPoD4) and in vitro enzyme activity assays.

Main Results:

  • Hypoxia increased dihydroceramide (DHC), dihydro-sphingosine (DH-Sph), DH-sphingosine1-phosphate (DH-S1P), DH-sphingomyelin (DH-SM), DH-glucosylceramide (DH-GlcCer), and sphingosine-1-phosphate (S1P) levels.
  • Increased glucosylceramide synthase (GCS) activity was observed, while sphingomyelinase and sphingomyelin synthase activities remained unchanged.
  • Inhibition of de novo sphingolipid synthesis or GCS exacerbated hypoxia-induced endothelial barrier dysfunction and apoptosis.

Conclusions:

  • Hypoxia induces the synthesis of S1P and various dihydro-sphingolipids in cerebral microendothelial cells.
  • These sphingolipids may possess vasculoprotective properties, potentially ameliorating stroke effects.
  • Targeting these pathways could offer therapeutic strategies for hypoxic conditions.