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Involvement of phosphatase and tensin homolog deleted from chromosome 10 in rodent model of neuropathic pain

Overview of attention for article published in Journal of Neuroinflammation, March 2015
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Title
Involvement of phosphatase and tensin homolog deleted from chromosome 10 in rodent model of neuropathic pain
Published in
Journal of Neuroinflammation, March 2015
DOI 10.1186/s12974-015-0280-1
Pubmed ID
Authors

Shi-Ying Huang, Chun-Sung Sung, Wu-Fu Chen, Chun-Hong Chen, Chien-Wei Feng, San-Nan Yang, Han-Chun Hung, Nan-Fu Chen, Pey-Ru Lin, San-Cher Chen, Hui-Min David Wang, Tian-Huei Chu, Ming-Hong Tai, Zhi-Hong Wen

Abstract

Many cancer research studies have extensively examined the phosphatase and tensin homolog deleted from chromosome 10 (PTEN) pathway. There are only few reports that suggest that PTEN might affect pain; however, there is still a lack of evidence to show the role of PTEN for modulating pain. Here, we report a role for PTEN in a rodent model of neuropathic pain. We found that chronic constriction injury (CCI) surgery in rats could elicit downregulation of spinal PTEN as well as upregulation of phosphorylated PTEN (phospho-PTEN) and phosphorylated mammalian target of rapamycin (phospho-mTOR). After examining such changes in endogenous PTEN in neuropathic rats, we explored the effects of modulating the spinal PTEN pathway on nociceptive behaviors. The normal rats exhibited mechanical allodynia after intrathecal (i.t.) injection of adenovirus-mediated PTEN antisense oligonucleotide (Ad-antisense PTEN). These data indicate the importance of downregulation of spinal PTEN for nociception. Moreover, upregulation of spinal PTEN by i.t. adenovirus-mediated PTEN (Ad-PTEN) significantly prevented CCI-induced development of nociceptive sensitization, thermal hyperalgesia, mechanical allodynia, cold allodynia, and weight-bearing deficits in neuropathic rats. Furthermore, upregulation of spinal PTEN by i.t. Ad-PTEN significantly attenuated CCI-induced microglia and astrocyte activation, upregulation of tumor necrosis factor-α (TNF-α) and phospho-mTOR, and downregulation of PTEN in neuropathic rats 14 days post injury. These findings demonstrate that PTEN plays a key, beneficial role in a rodent model of neuropathic pain.

Twitter Demographics

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Mendeley readers

The data shown below were compiled from readership statistics for 30 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 3%
Unknown 29 97%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 6 20%
Student > Ph. D. Student 6 20%
Student > Master 3 10%
Researcher 2 7%
Librarian 2 7%
Other 7 23%
Unknown 4 13%
Readers by discipline Count As %
Medicine and Dentistry 8 27%
Neuroscience 5 17%
Psychology 3 10%
Biochemistry, Genetics and Molecular Biology 2 7%
Environmental Science 2 7%
Other 5 17%
Unknown 5 17%

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 10 July 2016.
All research outputs
#6,121,030
of 8,058,126 outputs
Outputs from Journal of Neuroinflammation
#738
of 1,020 outputs
Outputs of similar age
#182,292
of 258,853 outputs
Outputs of similar age from Journal of Neuroinflammation
#41
of 53 outputs
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We're also able to compare this research output to 53 others from the same source and published within six weeks on either side of this one. This one is in the 15th percentile – i.e., 15% of its contemporaries scored the same or lower than it.