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FK506 prevents stroke-induced generation of ceramide and apoptosis signaling.

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Ceramide is a key mediator of apoptosis during the cellular stress response which is also involved in stroke-induced death. Transient occlusion of the middle cerebral artery (MCA) in rats led to a strong generation of ceramide as measured in thalamus and entorhinal cortex of the ischemic brain

Beta adrenoceptor blockade ameliorates impaired glucose tolerance and alterations of the cerebral ceramide metabolism in an experimental model of ischemic stroke.

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UNASSIGNED Sphingolipids are versatile signaling molecules derived from membrane lipids of eukaryotic cells. Ceramides regulate cellular processes such as proliferation, differentiation and apoptosis and are involved in cellular stress responses. Experimental evidence suggests a pivotal role of

Plasma levels of ceramides relate to ischemic stroke risk and clinical severity.

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Recent studies have suggested that specific plasma ceramides are independently associated with atherosclerosis and cardiovascular diseases, but it is currently unknown whether plasma ceramide levels are associated with ischemic stroke. Here, we examined whether ceramides were associated with both

Ceramides and sphingosine-1-phosphate as potential markers in diagnosis of ischaemic stroke.

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Brain imaging in stroke diagnostics is a powerful tool, but one that can fail in more challenging cases, and one that is not particularly useful in identifying transient ischaemic attacks (TIAs). Thus, new reliable blood biomarkers of cerebral ischaemia are constantly

The Acid Sphingomyelinase/ Ceramide System as Target for Ischemic Stroke Therapies.

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In this review, we summarize implications of the acid sphingomyelinase/ ceramide system in ischemic stroke. Acid sphingomyelinase catalyzes the formation of the bioactive sphingolipid ceramide which coalesces into membrane platforms and has a pivotal role in inflammation, cell signaling and death.

Sphingomyelinase and ceramide analogs induce vasoconstriction and leukocyte-endothelial interactions in cerebral venules in the intact rat brain: Insight into mechanisms and possible relation to brain injury and stroke.

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This study was designed to test the hypothesis that the sphingomyelin-ceramide signaling pathway may be important in proinflammatory-like responses in the intact brain. Effects of neutral sphingomyelinase (N-SMase), ceramide analogs, phosphorylcholine and ceramide metabolites were studied on rat

Anti-proliferative effects of tricyclodecan-9-yl-xanthogenate (D609) involve ceramide and cell cycle inhibition.

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Tricyclodecan-9-yl-xanthogenate (D609) inhibits phosphatidylcholine (PC)-phospholipase C (PLC) and/or sphingomyelin (SM) synthase (SMS). Inhibiting SMS can increase ceramide levels, which can inhibit cell proliferation. Here, we examined how individual inflammatory and glia cell proliferation is

Delayed metabolic dysfunction in myocardium following exertional heat stroke in mice.

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Exposure to exertional heat stroke (EHS) is associated with increased risk of long-term cardiovascular disorders in humans. We demonstrate that in female mice, severe EHS results in metabolic changes in the myocardium, emerging only after 9-14 days. This was not observed in males that

Sphingomyelinase-induced ceramide production stimulate calcium-independent JNK and PP2A activation following cerebral ischemia.

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OBJECTIVE Intracellular calcium overload is considered to be a key pathologic factor for ischemic stroke; however, there are other signal molecules produced in response to ischemic stimuli. The present study investigated the ceramide signal pathway, which is associated with cerebral ischemia in a

Hypoxic preconditioning protects cultured neurons against hypoxic stress via TNF-alpha and ceramide.

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Brief "preconditioning" ischemia induces ischemic tolerance (IT) and protects the animal brain from subsequent otherwise lethal ischemia. Identification of the signaling steps most proximal to the development of the IT will allow induction of the resistance to ischemia shortly after the onset of

Homocysteine induces cerebral endothelial cell death by activating the acid sphingomyelinase ceramide pathway.

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Homocysteine (Hcy) levels may rise after a stroke, but the mechanism of Hcy-induced cerebral endothelial cell (CEC) dysfunction has not been explored. In this study we examined the role of the acid sphingomyelinase (Asm)-ceramide pathway in the molecular mechanism of Hcy-induced CEC dysfunction.

[Value of ceramide in the diagnosis and risk prediction of coronary artery disease].

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Objective: To evaluate the clinical values of 4 types of ceramides (Cer1, Cer2, Cer3, Cer4) in the coronary artery stenosis, clinical diagnosis and risk prediction. Methods: A total of 890 patients with coronary heart disease (CHD) in Beijing Anzhen Hospital between March 2018 and

The protective effect of ceramide in immature rat brain hypoxia-ischemia involves up-regulation of bcl-2 and reduction of TUNEL-positive cells.

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Preconditioning brain with tumor necrosis factor alpha (TNF-alpha) can induce tolerance to experimental hypoxia and stroke and ceramide is a downstream messenger in the TNF-alpha signaling pathway. A hypoxic-ischemic (HI) insult in the immature rat injures brain primarily through apoptosis.

Fabry's disease presenting as stroke in a young female.

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BACKGROUND Fabry's disease is an X-linked disorder, caused by a deficiency of the lysosomal enzyme alpha-galactosidase A which results in the accumulation of the glycosphingolipid, ceramide trihexose in the vascular endothelium and can lead to cerebral infarction. Male hemizygotes are generally more

Plasma cerebrosides in stroke and multiple sclerosis.

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This investigation was conducted to determine whether or not plasma galactosyl ceramides were elevated in patients with stroke and multiple sclerosis, and to determine glycosyl ceramide concentrations in older, normal subjects. It was hypothesized that central nervous system destruction, like that

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