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dc.contributor.authorChartier, Stephane R
dc.contributor.authorMitchell, Stefanie AT
dc.contributor.authorMajuta, Lisa A
dc.contributor.authorMantyh, Patrick W
dc.date.accessioned2018-01-31T16:42:13Z
dc.date.available2018-01-31T16:42:13Z
dc.date.issued2017-11-22
dc.identifier.citationImmunohistochemical localization of nerve growth factor, tropomyosin receptor kinase A, and p75 in the bone and articular cartilage of the mouse femur 2017, 13:174480691774546 Molecular Painen
dc.identifier.issn1744-8069
dc.identifier.issn1744-8069
dc.identifier.pmid29166838
dc.identifier.doi10.1177/1744806917745465
dc.identifier.urihttp://hdl.handle.net/10150/626456
dc.description.abstractSequestration of nerve growth factor (NGF) significantly attenuates skeletal pain in both animals and humans. However, relatively little is known about the specific cell types that express NGF or its cognate receptors tropomyosin receptor kinase A (TrkA) and p75 in the intact bone and articular cartilage. In the present study, antibodies raised against NGF, TrkA, and p75 (also known as CD271) were used to explore the expression of these antigens in the non-decalcified young mouse femur. In general, all three antigens displayed a remarkably restricted expression in bone and cartilage with less than 2% of all DAPI+ cells in the femur displaying expression of any one of the three antigens. Robust NGF immunoreactivity was found in mostly CD-31- blood vessel-associated cells, a small subset of CD-31+ endothelial cells, an unidentified group of cells located at the subchondral bone/articular cartilage interface, and a few isolated, single cells in the bone marrow. In contrast, p75 and TrkA were almost exclusively expressed by nerve fibers located nearby NGF+ blood vessels. The only non-neuronal expression of either p75 or TrkA in the femur was the expression of p75 by a subset of cells located in the deep and middle zone of the articular cartilage. Understanding the factors that tightly regulate the basal level of expression in normal bone and how the expression of NGF, TrkA, and p75 change in injury, disease, and aging may provide insights into novel therapies that can reduce skeletal pain and improve skeletal health.
dc.description.sponsorshipNIH [CA154550, CA157449, NS023970]en
dc.language.isoenen
dc.publisherSAGE PUBLICATIONS INCen
dc.relation.urlhttp://journals.sagepub.com/doi/10.1177/1744806917745465en
dc.rights© The Author(s) 2017. This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License.en
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/
dc.subjectDecalcificationen
dc.subjectagingen
dc.subjectskeletonen
dc.subjectpainen
dc.subjectsensoryen
dc.subjectsympatheticen
dc.titleImmunohistochemical localization of nerve growth factor, tropomyosin receptor kinase A, and p75 in the bone and articular cartilage of the mouse femuren
dc.typeArticleen
dc.contributor.departmentUniv Arizona, Dept Pharmacolen
dc.contributor.departmentUniv Arizona, Canc Ctren
dc.identifier.journalMolecular Painen
dc.description.noteOpen access journal.en
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
dc.contributor.institutionDepartment of Pharmacology, University of Arizona, Tucson, AZ, USA
dc.contributor.institutionDepartment of Pharmacology, University of Arizona, Tucson, AZ, USA
dc.contributor.institutionDepartment of Pharmacology, University of Arizona, Tucson, AZ, USA
dc.contributor.institutionDepartment of Pharmacology, University of Arizona, Tucson, AZ, USA
refterms.dateFOA2018-09-12T01:08:36Z
html.description.abstractSequestration of nerve growth factor (NGF) significantly attenuates skeletal pain in both animals and humans. However, relatively little is known about the specific cell types that express NGF or its cognate receptors tropomyosin receptor kinase A (TrkA) and p75 in the intact bone and articular cartilage. In the present study, antibodies raised against NGF, TrkA, and p75 (also known as CD271) were used to explore the expression of these antigens in the non-decalcified young mouse femur. In general, all three antigens displayed a remarkably restricted expression in bone and cartilage with less than 2% of all DAPI+ cells in the femur displaying expression of any one of the three antigens. Robust NGF immunoreactivity was found in mostly CD-31- blood vessel-associated cells, a small subset of CD-31+ endothelial cells, an unidentified group of cells located at the subchondral bone/articular cartilage interface, and a few isolated, single cells in the bone marrow. In contrast, p75 and TrkA were almost exclusively expressed by nerve fibers located nearby NGF+ blood vessels. The only non-neuronal expression of either p75 or TrkA in the femur was the expression of p75 by a subset of cells located in the deep and middle zone of the articular cartilage. Understanding the factors that tightly regulate the basal level of expression in normal bone and how the expression of NGF, TrkA, and p75 change in injury, disease, and aging may provide insights into novel therapies that can reduce skeletal pain and improve skeletal health.


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© The Author(s) 2017. This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License.
Except where otherwise noted, this item's license is described as © The Author(s) 2017. This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License.