PMID- 27306411
OWN - NLM
STAT- MEDLINE
DCOM- 20161226
LR  - 20220331
IS  - 1744-8069 (Electronic)
IS  - 1744-8069 (Linking)
VI  - 12
DP  - 2016
TI  - EXPRESS: NGF-trkA signaling modulates the analgesic effects of prostatic acid 
      phosphatase in resiniferatoxin-induced neuropathy.
LID - 10.1177/1744806916656846 [doi]
LID - 1744806916656846
AB  - BACKGROUND: Neuropathic pain in small-fiber neuropathy results from injury to and 
      sensitization of nociceptors. Functional prostatic acid phosphatase (PAP) acts as 
      an analgesic effector. However, the mechanism responsible for the modulation of 
      PAP neuropathology, which leads to loss of the analgesic effect after small-fiber 
      neuropathy, remains unclear. RESULTS: We used a resiniferatoxin (RTX)-induced 
      small-fiber neuropathy model to examine whether functional PAP(thorn) neurons are 
      essential to maintain the analgesic effect. PAP(thorn) neurons were categorized into 
      small to medium neurons (25th-75th percentile: 17.1-23.7 mm); these neurons were 
      slightly reduced by RTX (p(1/4)0.0003). By contrast, RTX-induced activating 
      transcription factor 3 (ATF3), an injury marker, in PAP(thorn) neurons (29.0%5.6% vs. 
      0.2%0.2%, p(1/4)0.0043), indicating PAP neuropathology. Moreover, the high-affinity 
      nerve growth factor (NGF) receptor (trkA) colocalized with PAP and showed similar 
      profiles after RTX-induced neuropathy, and the PAP/trkA ratios correlated with 
      the degree of mechanical allodynia (r(1/4)0.62, p(1/4)0.0062). The NGF inducer 
      4-methylcatechol (4MC) normalized the analgesic effects of PAP; specifically, it 
      reversed the PAP and trkA profiles and relieved mechanical allodynia. 
      Administering 2.5S NGF showed similar results to those of administering 4MC. This 
      finding suggests that the analgesic effect of functional PAP is mediated by 
      NGF-trkA signaling, which was confirmed by NGF neutralization. CONCLUSIONS: This 
      study revealed that functional PAP(thorn) neurons are essential for the analgesic 
      effect, which is mediated by NGF-trkA signaling.
FAU - Wu, Chieh-Hsin
AU  - Wu CH
AD  - Kaohsiung Medical University Chung Ho Memorial Hospital.
FAU - Ho, Wan-Yi
AU  - Ho WY
AD  - Kaohsiung Medical University.
FAU - Lee, Yi-Chen
AU  - Lee YC
AD  - Kaohsiung Medical University.
FAU - Lin, Chih-Lung
AU  - Lin CL
AD  - Kaohsiung Medical University Hospital.
FAU - Hsieh, Yu-Lin
AU  - Hsieh YL
AD  - Kaohsiung Medical University Chung Ho Memorial HospitalKaohsiung Medical 
      UniversityKaohsiung Medical UniversityKaohsiung Medical University Hospital 
      ylhsieh@kmu.edu.tw.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160615
PL  - United States
TA  - Mol Pain
JT  - Molecular pain
JID - 101242662
RN  - 0 (Analgesics)
RN  - 0 (Catechols)
RN  - 0 (Diterpenes)
RN  - 0 (Receptors, Purinergic P2X3)
RN  - 12GLI7JGB3 (4-methylcatechol)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - A5O6P1UL4I (resiniferatoxin)
RN  - EC 2.7.10.1 (Receptor, trkA)
RN  - EC 3.1.3.2 (Acid Phosphatase)
RN  - EC 3.1.3.2 (prostatic acid phosphatase)
SB  - IM
MH  - Acid Phosphatase/*metabolism
MH  - Analgesics/*metabolism
MH  - Animals
MH  - Catechols
MH  - Diterpenes
MH  - Hyperalgesia/metabolism
MH  - Mice
MH  - Models, Biological
MH  - Nerve Growth Factor/*metabolism
MH  - Neuralgia/*chemically induced/*metabolism
MH  - Neurons/metabolism/pathology
MH  - Phenotype
MH  - Receptor, trkA/*metabolism
MH  - Receptors, Purinergic P2X3/metabolism
MH  - *Signal Transduction
PMC - PMC4956004
EDAT- 2016/06/17 06:00
MHDA- 2016/12/27 06:00
PMCR- 2016/06/15
CRDT- 2016/06/17 06:00
PHST- 2016/06/17 06:00 [entrez]
PHST- 2016/06/17 06:00 [pubmed]
PHST- 2016/12/27 06:00 [medline]
PHST- 2016/06/15 00:00 [pmc-release]
AID - 12/0/1744806916656846 [pii]
AID - 10.1177_1744806916656846 [pii]
AID - 10.1177/1744806916656846 [doi]
PST - epublish
SO  - Mol Pain. 2016 Jun 15;12:1744806916656846. doi: 10.1177/1744806916656846. Print 
      2016.