Matches in SemOpenAlex for { <https://semopenalex.org/work/W2076827306> ?p ?o ?g. }
Showing items 1 to 77 of
77
with 100 items per page.
- W2076827306 endingPage "S26" @default.
- W2076827306 startingPage "S26" @default.
- W2076827306 abstract "In response to various challenges, non-neuronal cells within the spinal cord become activated and increase dorsal horn neuronal excitability. While research in this area has focused on microglia and astrocytes, other cell types within the spinal cord are also likely to modulate pain transmission. We are investigating the possibility that signaling through toll-like receptors (TLRs) may activate endothelial cells and oligodendrocytes, and that these two cell types in the spinal cord might be an important source of pro-inflammatory cytokines and other neuroexcitatory substances that cause chronic pain and undermine opioid efficacy. Primary cultures were isolated from central nervous system tissue of adult male Sprague Dawley rats. Oligodendrocytes were obtained by immunopanning. Endothelial cells were obtained by culturing microvessels with puromycin, to eliminate contaminating cells. Endothelial cells exhibited basal TLR2 and TLR4 mRNA expression, and oligodendrocytes exhibited TLR2 only. Oligodendrocytes did not express detectable mRNA for IL-1β under basal conditions, but in response to stimulation with a TLR2 but not a TLR4 ligand, exhibited robust IL-1β mRNA expression. In response to stimulation with morphine in the presence of the free-radical spin trapping agent N-tert-butyl-a-phenylnitrone, endothelial cells exhibited upregulation of mRNA for IL-1β, iNOS, TNFα, COX-2 and MHC class II that was blocked by co-incubation with a TLR4 antagonist. Also, morphine or its metabolite morphine-3-glucuronide caused rapid and transient phosphorylation of p38 in endothelial cells. Ongoing studies are examining changes in sensitivity to TLR ligands in oligodendrocytes and endothelial cells isolated from animals with chronic pain or receiving chronic morphine. Our data suggest that endothelial cells and oligodendrocytes might modulate communication of pain messages via pro-inflammatory signaling, and may have a role in creating and maintaining chronic pain and undermining opioid efficacy. (Supported by NIH DA017670 and DA024044, and a Future Leaders in Pain Research grant from the American Pain Society.)" @default.
- W2076827306 created "2016-06-24" @default.
- W2076827306 creator A5011957342 @default.
- W2076827306 creator A5025282582 @default.
- W2076827306 creator A5046660513 @default.
- W2076827306 creator A5055356840 @default.
- W2076827306 creator A5061473424 @default.
- W2076827306 creator A5078472719 @default.
- W2076827306 date "2010-04-01" @default.
- W2076827306 modified "2023-10-14" @default.
- W2076827306 title "Pro-inflammatory signaling in endothelial cells and oligodendrocytes: new players in chronic pain and dysregulation of opioid efficacy" @default.
- W2076827306 doi "https://doi.org/10.1016/j.jpain.2010.01.110" @default.
- W2076827306 hasPublicationYear "2010" @default.
- W2076827306 type Work @default.
- W2076827306 sameAs 2076827306 @default.
- W2076827306 citedByCount "0" @default.
- W2076827306 crossrefType "journal-article" @default.
- W2076827306 hasAuthorship W2076827306A5011957342 @default.
- W2076827306 hasAuthorship W2076827306A5025282582 @default.
- W2076827306 hasAuthorship W2076827306A5046660513 @default.
- W2076827306 hasAuthorship W2076827306A5055356840 @default.
- W2076827306 hasAuthorship W2076827306A5061473424 @default.
- W2076827306 hasAuthorship W2076827306A5078472719 @default.
- W2076827306 hasBestOaLocation W20768273061 @default.
- W2076827306 hasConcept C125439840 @default.
- W2076827306 hasConcept C126322002 @default.
- W2076827306 hasConcept C170493617 @default.
- W2076827306 hasConcept C203014093 @default.
- W2076827306 hasConcept C24998067 @default.
- W2076827306 hasConcept C2776070231 @default.
- W2076827306 hasConcept C2776914184 @default.
- W2076827306 hasConcept C2777542381 @default.
- W2076827306 hasConcept C2779830541 @default.
- W2076827306 hasConcept C2781063702 @default.
- W2076827306 hasConcept C2781236682 @default.
- W2076827306 hasConcept C529278444 @default.
- W2076827306 hasConcept C71924100 @default.
- W2076827306 hasConcept C86803240 @default.
- W2076827306 hasConcept C88016717 @default.
- W2076827306 hasConcept C95444343 @default.
- W2076827306 hasConceptScore W2076827306C125439840 @default.
- W2076827306 hasConceptScore W2076827306C126322002 @default.
- W2076827306 hasConceptScore W2076827306C170493617 @default.
- W2076827306 hasConceptScore W2076827306C203014093 @default.
- W2076827306 hasConceptScore W2076827306C24998067 @default.
- W2076827306 hasConceptScore W2076827306C2776070231 @default.
- W2076827306 hasConceptScore W2076827306C2776914184 @default.
- W2076827306 hasConceptScore W2076827306C2777542381 @default.
- W2076827306 hasConceptScore W2076827306C2779830541 @default.
- W2076827306 hasConceptScore W2076827306C2781063702 @default.
- W2076827306 hasConceptScore W2076827306C2781236682 @default.
- W2076827306 hasConceptScore W2076827306C529278444 @default.
- W2076827306 hasConceptScore W2076827306C71924100 @default.
- W2076827306 hasConceptScore W2076827306C86803240 @default.
- W2076827306 hasConceptScore W2076827306C88016717 @default.
- W2076827306 hasConceptScore W2076827306C95444343 @default.
- W2076827306 hasIssue "4" @default.
- W2076827306 hasLocation W20768273061 @default.
- W2076827306 hasOpenAccess W2076827306 @default.
- W2076827306 hasPrimaryLocation W20768273061 @default.
- W2076827306 hasRelatedWork W1897355343 @default.
- W2076827306 hasRelatedWork W2021897449 @default.
- W2076827306 hasRelatedWork W2163169397 @default.
- W2076827306 hasRelatedWork W2217432868 @default.
- W2076827306 hasRelatedWork W2335592354 @default.
- W2076827306 hasRelatedWork W2363718755 @default.
- W2076827306 hasRelatedWork W2913512944 @default.
- W2076827306 hasRelatedWork W2947998877 @default.
- W2076827306 hasRelatedWork W2988640276 @default.
- W2076827306 hasRelatedWork W3032135212 @default.
- W2076827306 hasVolume "11" @default.
- W2076827306 isParatext "false" @default.
- W2076827306 isRetracted "false" @default.
- W2076827306 magId "2076827306" @default.
- W2076827306 workType "article" @default.