2009
DOI: 10.1016/j.jss.2008.08.021
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17β-Estradiol Activates Adenosine A2a Receptor After Subarachnoid Hemorrhage

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Cited by 22 publications
(19 citation statements)
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“…Due to its short half-life and quick desensitization, other upstream targets are currently being explored [78]. One example is estrogen, which significantly increases A 2A receptor expression [81]. Another agent, ORF4-PE, is a TNF-α-specific antisense oligodeoxynucleotide, and its intracerebral administration after ICH led to decrease in cell death and neurobehavioral deficits [82].…”
Section: Therapeutic Targets and Strategiesmentioning
confidence: 99%
“…Due to its short half-life and quick desensitization, other upstream targets are currently being explored [78]. One example is estrogen, which significantly increases A 2A receptor expression [81]. Another agent, ORF4-PE, is a TNF-α-specific antisense oligodeoxynucleotide, and its intracerebral administration after ICH led to decrease in cell death and neurobehavioral deficits [82].…”
Section: Therapeutic Targets and Strategiesmentioning
confidence: 99%
“…Recently, we found that, in neurones, Ngb was pivotal for hormone-induced anti-apoptotic effects against H2O2 toxicity, which may protect brain tissue from oxidative inflammatory injury [54], while E2 increased Ngb expression. (4)E2 has been found to exert antiapoptotic effects through upregulation of adenosine A2a receptor (A2aAR) and extracellular signal-regulated kinases 1 and 2 (ERK1/2) expression [55]. (5)The current in vivo evidence presented by Kao et al [56] implicates Akt signaling pathway in E2-mediated neuroprotection.…”
Section: Estrogenmentioning
confidence: 99%
“…This time window may allow for therapeutic intervention with TNF-α modulators, including adenosine receptor antagonists, estrogen, and anti-sense oligodeoxynucleotides such as ORF4-PE. These agents have been shown to decrease cell death, inflammation and neurobehavioral deficits [51][52][53].…”
Section: Tnf-αmentioning
confidence: 99%