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Expression of dual nucleotides/cysteinyl-leukotrienes receptor GPR17 in early trafficking of cardiac stromal cells after myocardial infarction.
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GPR17 is a G(i) -coupled dual receptor activated by uracil-nucleotides and cysteinyl-leukotrienes. These mediators are massively released into hypoxic tissues. In the normal heart, GPR17 expression has been reported. By contrast, its role in myocardial ischaemia has not yet been assessed. In the
A case of diffuse alveolar hemorrhage associated with tegafur plus uracil and warfarin therapy.
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A 72-year-old man who received warfarin for myocardial infarction (prothrombin time-international normalized ratio [PT-INR] controlled between 2.2 and 2.5) for 2 years. He developed lung cancer, underwent surgery, and received tegafur plus uracil (UFT) after 1 month. After 2 months, he was admitted
[Pseudouridine excretion with urine and RNA metabolism in experimental myocardial infarction and its correction].
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It is established that the acute period of the experimental myocardial infarction is characterized by an intensified excretion of pseudouridine with urine. Simultaneously in the "non-ischemic" area of the left cardiac ventricle as well as in the liver there occurs an activation of the transport and
[Cardiac toxicity of fluoro-uracil. Typical and atypical aspects. Apropos of 8 cases].
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The cardiac toxicity of 5 fluoro-uracil, an antimitotic agent widely used in various protocols, has been known for 16 years. Several cases have been reported in the literature, leading to the suggestion, without formal evidence, that the chief mechanism responsible for this cardiac toxicity is
Opposite effects of uracil and adenine nucleotides on the survival of murine cardiomyocytes.
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We previously showed that the human heart expresses all known P2X and P2Y receptors activated by extra-cellular adenine or uracil nucleotides. Despite evidence that, both in humans and rodents, plasma levels of ATP and UTP markedly increase during myocardial infarction, the differential effects
Increased postischemic brain injury in mice deficient in uracil-DNA glycosylase.
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Uracil-DNA glycosylase (UNG) is involved in base excision repair of aberrant uracil residues in nuclear and mitochondrial DNA. Ung knockout mice generated by gene targeting are viable, fertile, and phenotypically normal and have regular mutation rates. However, when exposed to a nitric oxide donor,
Uridine: a marker of myocardial viability after coronary occlusion and reperfusion.
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Tissue accumulation of radiolabeled uridine, a precursor of uracil, reflects ribonucleic acid (RNA) synthesis and may be a marker of viability. To test this hypothesis, myocardial accumulation of H-3 uridine was compared to deoxyglucose uptake and histopathology in an experimental model of
[Cardiogenic shock caused by 5-fluorouracil].
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The authors report the observation of one patient in whom the first administration of chemotherapy with fluoro-5 uracil has induced a severe but reversible cardiogenic shock. The latter was preceded by a prolonged, constrictive thoracic pain without myocardial infarction constitution. The cardiac
Mechanism of cardioprotective effect of orotic acid.
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The pyrimidine base, orotic acid (OA), markedly improves the function of recently infarcted hearts subjected to global ischemia. The mechanism of cardiac action of OA is unclear, but it has been proposed that OA acts by correcting a relative deficiency of nucleotide precursors required for RNA
[Cerebral ischemic events and anti-cancer therapy].
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Antineoplastic agents have been associated with cerebral hemorrhage, infarction and cerebral venous thrombosis. Infarctions have been reported in association with L-asparaginase, cisplatinium, methotrexate and 5-fluro-uracil. The mechanisms by which antineoplastic agents may lead to stroke include
Cardioprotection by orotic acid: metabolism and mechanism of action.
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The pyrimidine base, orotic acid (OA), improves the function of recently infarcted hearts subjected to global ischemia but its mechanism of action is unclear. Our aims were to examine (i) in normal rats, the effect of OA on pyrimidine levels in plasma, liver and heart; (ii) in rats with normal or
Folate deficiency increases postischemic brain injury.
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OBJECTIVE
Folate deficiency and resultant hyperhomocysteinemia impair vascular function and increase stroke risk. We tested the hypothesis that folate deficiency and high homocysteine levels promote DNA damage and increase brain injury after cerebral ischemia/reperfusion.
METHODS
129/Sv mice,
The new P2Y-like receptor G protein-coupled receptor 17 mediates acute neuronal injury and late microgliosis after focal cerebral ischemia in rats.
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G protein-coupled receptor 17 (GPR17), the new P2Y-like receptor, is phylogenetically related to the P2Y and cysteinyl leukotriene receptors, and responds to both uracil nucleotides and cysteinyl leukotrienes. GPR17 has been proposed to be a damage sensor in ischemic stroke; however, its role in
Up-regulation of myocardial DNA base excision repair activities in experimental heart failure.
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Base excision repair (BER) is the major pathway to counteract the genotoxic effect of endogenous DNA damaging agents. The present study investigated the enzymatic activities and gene transcription of DNA glycosylases initiating BER in an experimental heart failure (HF) model. Rats were subjected to
The recently identified P2Y-like receptor GPR17 is a sensor of brain damage and a new target for brain repair.
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Deciphering the mechanisms regulating the generation of new neurons and new oligodendrocytes, the myelinating cells of the central nervous system, is of paramount importance to address new strategies to replace endogenous damaged cells in the adult brain and foster repair in neurodegenerative
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