ArticleMolecular medicine reports2018
The association between the expression of PAR2 and TMEM16A and neuropathic pain.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- TMEM16A Activation Inhibits Autophagy in Dorsal Root Ganglion Cells, Which is Associated with the p38 MAPK/mTOR Pathway.Cellular and molecular neurobiology · 2024Article
- The role of anoctamin 1 in liver disease.Journal of cellular and molecular medicine · 2024Review
- Single-Nucleotide Polymorphisms of theInternational journal of molecular sciences · 2023Article
- Positive interaction between GPER and β-alanine in the dorsal root ganglion uncovers potential mechanisms: mediating continuous neuronal sensitization and neuroinflammation responses in neuropathic pain.Journal of neuroinflammation · 2022Article
- The diverse roles of TMEM16A CaJournal of advanced research · 2021Review
- The Role of TMEM16A/ERK/NK-1 Signaling in Dorsal Root Ganglia Neurons in the Development of Neuropathic Pain Induced by Spared Nerve Injury (SNI).Molecular neurobiology · 2021Article
- The CaActa pharmaceutica Sinica. B · 2021Review
- Upregulation of miR-144-3p protects myocardial function from ischemia-reperfusion injury through inhibition of TMEM16A CaHuman cell · 2021Article
- Upregulation of Nav1.7 by endogenous hydrogen sulfide contributes to maintenance of neuropathic pain.International journal of molecular medicine · 2020Article
- Chloride - The Underrated Ion in Nociceptors.Frontiers in neuroscience · 2020Review
- Age‑associated variation in the expression and function of TMEM16A calcium‑activated chloride channels in the cochlear stria vascularis of guinea pigs.Molecular medicine reports · 2019Article
- Mechanism of persistent hyperalgesia in neuropathic pain caused by chronic constriction injury.Neural regeneration research · 2019Article
- Nociceptor Signalling through ion Channel Regulation via GPCRs.International journal of molecular sciences · 2019Review
- 17β-Estradiol Attenuates Neuropathic Pain Caused by Spared Nerve Injury by Upregulating CIC-3 in the Dorsal Root Ganglion of Ovariectomized Rats.Frontiers in neuroscience · 2019Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic constriction injury (CCI) of the sciatic nerve may induce dorsal root ganglion (DRG) neuronal hyperexcitability and behaviorally expressed hyperalgesia. CCI is a model of neuropathic pain. To investigate the association between the expression of protease activated receptor 2 (PAR2), TMEM16A and neuropathic pain, the expression of PAR2 and TMEM16A proteins in the DRG neurons of rats following CCI of the sciatic nerve was investigated. Following the creation of the CCI model, the thermal withdrawal latency (TWL) was examined by a hot plate test. An immunofluorescence assay and western blot assay were performed to determine the expression of PAR2 and TMEM16A proteins in the ipsilateral L4‑6 DRG neurons. The concentration of inositol 1,4,5‑triphosphate (IP3) in the L4‑6 DRG was determined by ELISA. In the CCI‑D7 (7 days after CCI) and CCI‑D14 (14 days after CCI) treatment groups, the TWL of rats was significantly shorter than that in the sham operated group (P<0.01; n=12). The expression of PAR2 and TMEM16A proteins in the CCI‑D7 and CCI‑D14 groups were significantly upregulated compared with the sham operated group (P<0.05; n=12). Additionally, it was revealed that PAR2 and TMEM16A were co‑expressed in DRG neurons. It was also observed that IP3 significantly increased in the CCI‑D7 and CCI‑D14 groups compared with the sham operation group (P<0.05; n=6) as PAR2 and TMEM16A also increased. These findings suggest that the upregulation of PAR2 and TMEM16A in DRG neurons, the co‑expression of the two proteins and increasing IP3 are critical to the development of neuropathic pain.
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