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Keratinocyte expression of inflammatory mediators plays a crucial role in substance P-induced acute and chronic pain

Overview of attention for article published in Journal of Neuroinflammation, July 2012
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Title
Keratinocyte expression of inflammatory mediators plays a crucial role in substance P-induced acute and chronic pain
Published in
Journal of Neuroinflammation, July 2012
DOI 10.1186/1742-2094-9-181
Pubmed ID
Authors

Tzuping Wei, Tian-Zhi Guo, Wen-Wu Li, Saiyun Hou, Wade S Kingery, John David Clark

Abstract

Tibia fracture in rats followed by cast immobilization leads to nociceptive, trophic, vascular and bone-related changes similar to those seen in Complex Regional Pain Syndrome (CRPS). Substance P (SP) mediated neurogenic inflammation may be responsible for some of the signs of CRPS in humans. We therefore hypothesized that SP acting through the SP receptor (NK1) leads to the CRPS-like changes found in the rat model. In the present study, we intradermally injected rats with SP and monitored hindpaw mechanical allodynia, temperature, and thickness as well as tissue levels of tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), interleukin 6 (IL-6), and nerve growth factor-β (NGF) for 72 h. Anti-NGF antibody was utilized to block the effects of SP-induced NGF up-regulation. Fracture rats treated with the selective NK1 receptor antagonist LY303870 prior to cast removal were assessed for BrdU, a DNA synthesis marker, incorporation in skin cells to examine cellular proliferation. Bone microarchitecture was measured using micro computed tomography (μCT). We observed that: (1) SP intraplantar injection induced mechanical allodynia, warmth and edema as well as the expression of nociceptive mediators in the hindpaw skin of normal rats, (2) LY303870 administered intraperitoneally after fracture attenuated allodynia, hindpaw unweighting, warmth, and edema, as well as cytokine and NGF expression, (3) LY303870 blocked fracture-induced epidermal thickening and BrdU incorporation after fracture, (4) anti-NGF antibody blocked SP-induced allodynia but not warmth or edema, and (5) LY303870 had no effect on bone microarchitecture. Collectively our data indicate that SP acting through NK1 receptors supports the nociceptive and vascular components of CRPS, but not the bone-related changes.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 60 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 2 3%
Russia 1 2%
Brazil 1 2%
Unknown 56 93%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 15 25%
Student > Master 9 15%
Researcher 6 10%
Other 6 10%
Professor > Associate Professor 4 7%
Other 13 22%
Unknown 7 12%
Readers by discipline Count As %
Agricultural and Biological Sciences 20 33%
Neuroscience 12 20%
Medicine and Dentistry 9 15%
Pharmacology, Toxicology and Pharmaceutical Science 3 5%
Biochemistry, Genetics and Molecular Biology 2 3%
Other 5 8%
Unknown 9 15%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 14 October 2012.
All research outputs
#17,661,224
of 22,671,366 outputs
Outputs from Journal of Neuroinflammation
#1,921
of 2,605 outputs
Outputs of similar age
#121,375
of 164,297 outputs
Outputs of similar age from Journal of Neuroinflammation
#46
of 60 outputs
Altmetric has tracked 22,671,366 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,605 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.6. This one is in the 21st percentile – i.e., 21% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 164,297 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 23rd percentile – i.e., 23% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 60 others from the same source and published within six weeks on either side of this one. This one is in the 18th percentile – i.e., 18% of its contemporaries scored the same or lower than it.