Amino acid release into the knee joint: key role in nociception and inflammation

Lawand, Nada; McNearney, Terry A.; Westlund, Karin N.

doi:10.1016/s0304-3959(99)00311-5

Cited by 154 publications

(104 citation statements)

References 47 publications

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“…Peripheral nerves release transmitters and peptides, including CGRP (Lam and Ferrell, 1991;Mulder et al, 1997;Lawand et al, 2000). Unilateral inflammation causes alterations in nociceptive thresholds (Stein et al, 1988), and notably, mice deficient in the ␣-CGRP gene fail to develop secondary hyperalgesia after inflammation (Zhang et al, 2001).…”

Section: Inflammation Increases Sensory Neuropeptides and Painmentioning

confidence: 99%

Activin Induces Tactile Allodynia and Increases Calcitonin Gene-Related Peptide after Peripheral Inflammation

Slambrouck

Berti‐Mattera

et al. 2005

J. Neurosci.

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Calcitonin gene-related peptide (CGRP) is a sensory neuropeptide important in inflammatory pain that conveys pain information centrally and dilates blood vessels peripherally. Previous studies indicate that activin A increases CGRP-immunoreactive (IR) sensory neurons in vitro, and following wound, activin A protein increases in the skin and more neurons have detectable CGRP expression in the innervating dorsal root ganglion (DRG). These data suggest some adult sensory neurons respond to activin A or other target-derived factors with increased neuropeptide expression. This study was undertaken to test whether activin contributes to inflammatory pain and increased CGRP and to learn which neurons retained plasticity. After adjuvant-induced inflammation, activin mRNA, but not NGF or glial cell line-derived neurotrophic factor, increased in the skin. To examine which DRG neurons increased CGRP immunoreactivity, retrograde tracer-labeled cutaneous neurons were characterized after inflammation. The proportion and size of tracer-labeled DRG neurons with detectable CGRP increased after inflammation. One-third of CGRP-IR neurons that appear after inflammation also had isolectin B4 binding, suggesting that some mechanoreceptors became CGRP-IR. In contrast, the increased proportion of CGRP-IR neurons did not appear to come from RT97-IR neurons. To learn whether central projections were altered after inflammation, CGRP immunoreactivity in the protein kinase C␥-IR lamina IIi was quantified and found to increase. Injection of activin A protein alone caused robust tactile allodynia and increased CGRP in the DRG. Together, these data support the hypothesis that inflammation and skin changes involving activin A cause some sensory neurons to increase CGRP expression and pain responses.

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Section: Inflammation Increases Sensory Neuropeptides and Painmentioning

confidence: 99%

Activin Induces Tactile Allodynia and Increases Calcitonin Gene-Related Peptide after Peripheral Inflammation

Slambrouck

Berti‐Mattera

et al. 2005

J. Neurosci.

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“…41 Intraarticular EAA injection resulted in thermal hyperalgesia and mechanical allodynia, which were attenuated by local injection of N-methyl-D-aspartate (NMDA) or non-NMDA receptor antagonists. 27 Lawand et al 26 also demonstrated that intraarticular lidocaine injection prevented glutamate release and nociceptors sensitization of inflammatory joints. Moreover, in inflamed arthritic knees, an increase of glutamate concentration was observed not only in the axons in the inflamed region, 25 but also in the synovial fluid.…”

Section: Discussionmentioning

confidence: 94%

“…A 27-gauge needle attached to a tuberculin syringe was passed through the joint capsule lateral to the patellar ligament, then the microdialysis probe was inserted through the needle into the knee joint, following the protocol described by Lawand et al, 26 and its position confirmed by X-ray examination. The microdialysis probe 28 was constructed using two 5-cm polyethylene tubes (0.008-inch inner diameter, 0.014-inch outer diameter) and a 1.5-cm cuprophan hollow fiber (300 mm outer diameter, 200 mm inner diameter, 50 kDa molecular weight cutoff; Filtral, AN 69-HF, Eicom Co., Kyoto, Japan).…”

Section: Construction and Placement Of The Microdialysis Probementioning

confidence: 99%

“…25 A potential peripheral action of glutamate has been suggested, as increased glutamate levels are seen in the peripheral tissues in acute and chronic inflammation in both animals and humans. 23,26,27 Increased glutamate levels in the knee joint and medial articular nerve are seen after induction of arthritis in the rat. 26 We previously reported that glutamate and aspartate levels were significantly increased in dialysates of anterior cruciate ligament-transected (ACLT) knees, 28 suggesting a role of EAA in early OA development.…”

Section: Introductionmentioning

confidence: 99%

“…23,26,27 Increased glutamate levels in the knee joint and medial articular nerve are seen after induction of arthritis in the rat. 26 We previously reported that glutamate and aspartate levels were significantly increased in dialysates of anterior cruciate ligament-transected (ACLT) knees, 28 suggesting a role of EAA in early OA development. Glutamate transporters have been identified in bone, 29 raising the possibility that EAA participate in signal transduction between bone cells.…”

Section: Introductionmentioning

confidence: 99%

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Hyaluronic acid attenuates osteoarthritis development in the anterior cruciate ligament‐transected knee: Association with excitatory amino acid release in the joint dialysate

Jean

Wen

Chang

et al. 2006

Journal Orthopaedic Research

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We previously reported increased release of the excitatory amino acid (EAA) neurotransmitters, glutamate and aspartate, during the early stage of experimental osteoarthritis (OA). Our present objective was to study the effect of intraarticular injection of hyaluronic acid (HA) on OA development, and to analyze concomitant changes in EAA levels in dialysates of anterior cruciate ligament-transected (ACLT) knee joints. OA was induced in Wistar rats by ACLT of one hindlimb; the knee of the other hindlimb was used as the sham-operated control. HA group (n ¼ 12) were injected intraarticularly in the ACLT knee with 1 mg of HA once a week for 5 consecutive weeks, starting at 8 weeks after surgery. Saline group (n ¼ 12) were injected as above with normal saline. The sham-operated group, underwent arthrotomy, but not ACLT, and received no treatment (n ¼ 14). Twenty weeks after surgery, knee joint dialysates were collected by microdialysis and EAA levels assayed by high-performance liquid chromatography, and gross morphological examination and histopathological evaluation were performed on the medial femoral condyles and synovia. Rats receiving intraarticular HA injections showed a significantly lower degree of cartilage degeneration on the medial femoral condyle at both the macroscopic level and on the Mankin grading scale than rats receiving saline injections. Intraarticular HA treatment also suppressed synovitis. Moreover, glutamate and aspartate levels were significantly reduced in the HA group compared to the saline group. Intraarticular injection of HA limits articular cartilage and synovium damage and OA formation, and, in parallel, reduces EAA levels in ACLT joint dialysates. This study suggests that the underlying mechanism of the anti-inflammatory effect of HA is to inhibit glutamate and aspartate release in ACLT knee joints, which attenuates the early development of OA. ß

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Characterization of phosphoproteins from electrophoretic gels by nanoscale Fe(III) affinity chromatography with off-line mass spectrometry analysis

2001

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Detailed characterization of phosphoproteins as well as other post-translationally modified proteins is required to fully understand protein function and regulatory events in cells and organisms. Here we present a mass spectrometry (MS) based experimental strategy for the identification and mapping of phosphorylation site(s) using only low-picomole amounts of phosphoprotein starting material. Miniaturized sample preparation methods for MS facilitated localization of phosphorylation sites in phosphoproteins isolated by polyacrylamide gel electrophoresis. Custom made, nanoscale immobilized Fe(III) affinity chromatography (Fe(III)-IMAC) columns were employed for enrichment of phosphorylated peptides from crude peptide mixtures prior to off-line analysis by matrix-assisted laser desorption/ionization (MALDI) MS or nanoelectrospray tandem mass spectrometry (MS/MS). An optimized and sensitive procedure for alkaline phosphatase treatment of peptide mixtures was implemented, which in combination with nano-scale Fe(III)-IMAC and MALDI-MS allowed unambiguous identification of phosphopeptides by observation of 80 Da mass shifts. Nanoelectrospray MS/MS was used for phosphopeptide sequencing for exact determination of phosphorylation sites. The advantages and limitations of the experimental strategy was demonstrated by enrichment, identification and sequencing of phosphopeptides from the model proteins ovalbumin and bovine beta-casein isolated by gel electrophoresis. Furthermore, an autophosphorylation site at Ser-3 in recombinant human casein kinase-2 beta subunit was determined. The potential of miniaturized Fe(III)-IMAC and MALDI-MS for characterization of in vivo phosphorylated proteins was demonstrated by identification of tryptic phosphopeptides derived from the human p47/phox phosphoprotein isolated by two-dimensional gel electrophoresis.

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Amino acid release into the knee joint: key role in nociception and inflammation

Cited by 154 publications

References 47 publications

Activin Induces Tactile Allodynia and Increases Calcitonin Gene-Related Peptide after Peripheral Inflammation

Activin Induces Tactile Allodynia and Increases Calcitonin Gene-Related Peptide after Peripheral Inflammation

Hyaluronic acid attenuates osteoarthritis development in the anterior cruciate ligament‐transected knee: Association with excitatory amino acid release in the joint dialysate

Characterization of phosphoproteins from electrophoretic gels by nanoscale Fe(III) affinity chromatography with off-line mass spectrometry analysis

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