Linked Life Data

19660865

Source:http://linkedlifedata.com/resource/pubmed/id/19660865

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-9-11
pubmed:abstractText
Substance P (SP) signaling facilitates nociceptive sensitization in various inflammatory and chronic pain models and we postulated that SP signaling might also contribute to the development of post-incisional hyperalgesia. These studies used mice with a deletion of the pre-protachykinin A gene (ppt-A(-/-)) which codes for SP to determine the role of SP signaling in post-incisional pain and in the increased cytokine and nerve growth factor (NGF) expression observed in the incised skin. SP deficient ppt-A(-/-) mice displayed reduced mechanical allodynia and heat hyperalgesia compared to the wild-type (wt) mice at all post-incision time points, despite similar baseline values (p<0.001). Furthermore, the NK-1 receptor antagonist LY303870 attenuated mechanical allodynia produced by incision in the wt mice (p<0.001). Incision also up-regulated IL-6, TNF-alpha and KC levels but not IL-1beta after 2h in the wt mice skin. However, ppt-A(-/-) mice had more skin NGF levels 2h post-incision. Subcutaneous hind paw SP injection produced acute and transient elevations of IL-1beta, IL-6, and KC but modest elevations in TNF-alpha levels in the wt mice. Systemic LY303870 reversed the SP-induced elevations of these cytokines. Hind paw injection of IL-6 and NGF dose dependently produced less mechanical allodynia in the ppt-A(-/-) compared to wt mice. Additionally, SP produced mechanical allodynia in a dose-dependent fashion in wt mice. Therefore, SP supports nociceptive sensitization after hind paw incision and potentially participates directly in modulating the intensity of inflammatory response in peri-incisional tissue.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1872-6623
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
145
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
341-9
pubmed:dateRevised
2011-3-29
pubmed:meshHeading
pubmed-meshheading:19660865-Analysis of Variance, pubmed-meshheading:19660865-Animals, pubmed-meshheading:19660865-Cytokines, pubmed-meshheading:19660865-Disease Models, Animal, pubmed-meshheading:19660865-Dose-Response Relationship, Drug, pubmed-meshheading:19660865-Gene Expression Regulation, pubmed-meshheading:19660865-Hyperalgesia, pubmed-meshheading:19660865-Indoles, pubmed-meshheading:19660865-Male, pubmed-meshheading:19660865-Mice, pubmed-meshheading:19660865-Mice, Inbred C57BL, pubmed-meshheading:19660865-Mice, Knockout, pubmed-meshheading:19660865-Nerve Growth Factor, pubmed-meshheading:19660865-Pain, Postoperative, pubmed-meshheading:19660865-Pain Measurement, pubmed-meshheading:19660865-Pain Threshold, pubmed-meshheading:19660865-Piperidines, pubmed-meshheading:19660865-Protein Precursors, pubmed-meshheading:19660865-Receptors, Neurokinin-1, pubmed-meshheading:19660865-Signal Transduction, pubmed-meshheading:19660865-Substance P, pubmed-meshheading:19660865-Tachykinins, pubmed-meshheading:19660865-Time Factors
pubmed:year
2009
pubmed:articleTitle
Role of substance P signaling in enhanced nociceptive sensitization and local cytokine production after incision.
pubmed:affiliation
Department of Anesthesia, Stanford University School of Medicine, Stanford, CA, USA. psahbaie@stanford.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural