PMID- 31032956
OWN - NLM
STAT- MEDLINE
DCOM- 20200601
LR  - 20200601
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 234
IP  - 11
DP  - 2019 Nov
TI  - P2Y(14) receptor is functionally expressed in satellite glial cells and mediates 
      interleukin-1beta and chemokine CCL2 secretion.
PG  - 21199-21210
LID - 10.1002/jcp.28726 [doi]
AB  - Satellite glial cells (SGCs) activation in the trigeminal ganglia (TG) is 
      critical in various abnormal orofacial sensation in nerve injury and inflammatory 
      conditions. SGCs express several subtypes of P2 purinergic receptors contributing 
      to the initiation and maintenance of neuropathic pain. The P2Y(14) receptor, a 
      G-protein-coupled receptor activated by uridine diphosphate (UDP)-glucose and 
      other UDP sugars, mediates various physiologic events such as immune, 
      inflammation, and pain. However, the expression, distribution, and function of 
      P2Y(14) receptor in SGCs remains largely unexplored. Our study reported the 
      expression and functional identification of P2Y(14) receptor in SGCs. SGCs were 
      isolated from TG of rat, and the P2Y(14) receptor expression was examined using 
      immunofluorescence technique. Cell proliferation and viability were examined via 
      cell counting kit-8 experiment. Immunofluorescence demonstrated the presence of 
      P2Y(14) receptor in SGCs. Immunofluorescence and western blot showed that 
      UDP-glucose treatment upregulated glial fibrillary acid protein, a common marker 
      for glial activation. Extracellular UDP-glucose enhanced the phosphorylation of 
      extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and 
      p38, which were both abolished by the P2Y(14) receptor inhibitor (PPTN). 
      Furthermore, quantitative reverse transcription polymerase chain reaction and 
      enzyme-linked immunosorbent assay demonstrated that extracellular UDP-glucose 
      significantly enhanced interleukin-1beta (IL-1beta) and chemokine CCL2 (CCL2) release, 
      which was abolished by PPTN and significantly decreased by inhibitors of MEK/ERK 
      (U0126) and p38 (SB202190). Our findings directly proved the functional presence 
      of P2Y(14) receptor in SGCs. It was also verified that P2Y(14) receptor 
      activation was involved in activating SGCs, phosphorylating MAPKs, and promoting 
      the secretion of IL-1beta and CCL2 via ERK and p38 pathway.
CI  - (c) 2019 Wiley Periodicals, Inc.
FAU - Lin, Jiu
AU  - Lin J
AUID- ORCID: 0000-0003-0034-9686
AD  - State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral 
      Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
FAU - Liu, Fei
AU  - Liu F
AD  - State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral 
      Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
FAU - Zhang, Yan-Yan
AU  - Zhang YY
AD  - State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral 
      Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
FAU - Song, Ning
AU  - Song N
AD  - State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral 
      Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
FAU - Liu, Meng-Ke
AU  - Liu MK
AD  - State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral 
      Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
FAU - Fang, Xin-Yi
AU  - Fang XY
AD  - State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral 
      Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
FAU - Liao, Da-Qing
AU  - Liao DQ
AD  - Laboratory of Anesthesia & Critical Care Medicine, Translational Neuroscience 
      Center, West China Hospital of Sichuan University, Chengdu, China.
FAU - Zhou, Cheng
AU  - Zhou C
AD  - Laboratory of Anesthesia & Critical Care Medicine, Translational Neuroscience 
      Center, West China Hospital of Sichuan University, Chengdu, China.
FAU - Wang, Hang
AU  - Wang H
AD  - State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral 
      Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
FAU - Shen, Jie-Fei
AU  - Shen JF
AD  - State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral 
      Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190429
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1beta)
RN  - 0 (P2Y14 receptor, rat)
RN  - 0 (Receptors, Purinergic P2Y)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/*metabolism
MH  - Interleukin-1beta/*metabolism
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Purinergic P2Y/*metabolism
MH  - Satellite Cells, Perineuronal/*metabolism
OTO - NOTNLM
OT  - P2Y14 receptor
OT  - Satellite glial cells
OT  - chemokine CCL2
OT  - interleukin-1beta
OT  - mitogen-activated protein kinases
EDAT- 2019/04/30 06:00
MHDA- 2020/06/02 06:00
CRDT- 2019/04/30 06:00
PHST- 2018/11/26 00:00 [received]
PHST- 2019/04/08 00:00 [revised]
PHST- 2019/04/10 00:00 [accepted]
PHST- 2019/04/30 06:00 [pubmed]
PHST- 2020/06/02 06:00 [medline]
PHST- 2019/04/30 06:00 [entrez]
AID - 10.1002/jcp.28726 [doi]
PST - ppublish
SO  - J Cell Physiol. 2019 Nov;234(11):21199-21210. doi: 10.1002/jcp.28726. Epub 2019 
      Apr 29.