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- aggregation classification "A1".
- aggregation creator B385075.
- aggregation creator B385076.
- aggregation creator B385077.
- aggregation creator person.
- aggregation date "2010".
- aggregation format "application/pdf".
- aggregation hasFormat 940429.bibtex.
- aggregation hasFormat 940429.csv.
- aggregation hasFormat 940429.dc.
- aggregation hasFormat 940429.didl.
- aggregation hasFormat 940429.doc.
- aggregation hasFormat 940429.json.
- aggregation hasFormat 940429.mets.
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- aggregation hasFormat 940429.txt.
- aggregation hasFormat 940429.xls.
- aggregation hasFormat 940429.yaml.
- aggregation isPartOf urn:issn:0007-0912.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Pharmacology of capsaicin-, anandamide-, and N-arachidonoyl-dopamine-evoked cell death in a homogeneous transient receptor potential vanilloid subtype 1 receptor population".
- aggregation abstract "Background. Transient receptor potential vanilloid subtype 1 (TRPV1) receptor is a primary pain-sensing relay at peripheral sensory nerve endings and is also widespread in the brain, where it is implicated in neurodegeneration. Previous studies of TRPV1 neurotoxicity have utilized heterogeneous receptor populations, non-selective ligands, or non-neuronal cell types. Here, we explored the pharmacology of TRPV1-induced cytotoxicity in a homogeneous, neurone-like cellular environment. Methods. Cell death was examined in a human neurone-like cell line, stably expressing recombinant human TRPV1. Cytotoxicity was quantified in terms of nuclear morphology and mitochondrial complex II activity. Immunocytochemical markers of apoptotic cell death were also examined. Results. The TRPV1-selective agonist capsaicin, and the endovanilloids anandamide and N-arachidonoyl-dopamine (NADA), induced TRPV1-dependent delayed cell death in a concentration- and time-dependent manner. Capsaicin exposure time was significantly correlated with potency (r2¼0.91, P¼0.01). Release of cytochrome c from mitochondria, activation of caspase-3, and condensed nuclear chromatin were evident 6 h after capsaicin exposure, but cytotoxicity was unaffected by a pan-caspase inhibitor (zVAD-fmk, 50 mM). Conclusions. We conclude that capsaicin, anandamide, and NADA can initiate TRPV1-dependent delayed cell death in neurone-like cells. This is an apoptosis-like process, but independent of caspase activity.".
- aggregation authorList BK696116.
- aggregation endPage "602".
- aggregation issue "5".
- aggregation startPage "596".
- aggregation volume "104".
- aggregation aggregates 2937317.
- aggregation isDescribedBy 940429.
- aggregation similarTo aeq067.
- aggregation similarTo LU-940429.