ArticlePharmacology research & perspectives2016
Diclofenac, a nonsteroidal anti-inflammatory drug, is an antagonist of human TRPM3 isoforms.
Article in Pharmacology research & perspectives, 2016. 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, 32 citations in OpenAlex.
- Sex difference in TRPM3 channel functioning in nociceptive and vascular systems: an emerging target for migraine therapy in females?The journal of headache and pain · 2025Review
- Targeting TRPM3 as a potential therapeutic approach for autosomal dominant polycystic kidney disease.Scientific reports · 2025Article
- Anesthetic- and Analgesic-Related Drugs Modulating Both Voltage-Gated NaBiomolecules · 2024Review
- Navigating the Controversies: Role of TRPM Channels in Pain States.International journal of molecular sciences · 2024Review
- TRPM3, TRPM4, and TRPM5 as thermo-sensitive channels.The journal of physiological sciences : JPS · 2024Review
- Pharmacological properties of TRPM3 isoforms are determined by the length of the pore loop.British journal of pharmacology · 2022Article
- Topical Treatments and Their Molecular/Cellular Mechanisms in Patients with Peripheral Neuropathic Pain-Narrative Review.Pharmaceutics · 2021Review
- TRPM3 in Brain (Patho)Physiology.Frontiers in cell and developmental biology · 2021Review
- Inhibition of Fast Nerve Conduction Produced by Analgesics and Analgesic Adjuvants-Possible Involvement in Pain Alleviation.Pharmaceuticals (Basel, Switzerland) · 2020Review
- TRPM3_miR-204: a complex locus for eye development and disease.Human genomics · 2020Review
- Identification and classification of a new TRPM3 variant (γ subtype).The journal of physiological sciences : JPS · 2019Article
- Sensing the heat with TRPM3.Pflugers Archiv : European journal of physiology · 2018Review
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- Diclofenac, a nonsteroidal anti-inflammatory drug, is an antagonist of human TRPM3 isoforms.Pharmacology research & perspectives · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of diclofenac (Dic), an acetic acid derivative-type nonsteroidal anti-inflammatory drug, were examined on the function of transient receptor potential (TRP) melastatin (TRPM) 3 (TRPM3) in human embryonic kidney 293 cell-line (HEK293) cells with recombinant human TRPM3 isoforms (TRPM31325, TRPM3-3, TRPM3-9, and TRPM3-S) and in a neuroblastoma cell line human neuroblastoma IMR-32 cells (IMR-32 cells) derived from human peripheral neurons. TRPM3 responses evoked by pregnenolone sulfate (PregS) were effectively inhibited by Dic in a concentration-dependent manner in Ca(2+) measurement and electrophysiological assays. The apparent IC 50 for PregS-induced Ca(2+) response of TRPM31325, TRPM3-3, and TRPM3-9 was calculated to be 18.8, 42.5, and 7.1 μmol/L, respectively. The TRPM3-dependent Ca(2+) responses evoked by nifedipine, another TRPM3 agonist, were also significantly inhibited by Dic. In contrast, aceclofenac, an acetoxymethyl analog of Dic, had no effects on PregS-induced TRPM3 responses. Constitutive channel activity of TRPM3-S without TRPM3 agonists was substantially inhibited by Dic, ruling out the possibility of interaction of Dic against TRPM3 agonists to the channel binding sites. Moreover, Dic reversibly inhibited TRPM3 single-channel activity recorded in excised outside-out patches without affecting the channel conductance. In differentiated neuronal IMR-32 cells with endogenous TRPM3, Dic inhibited PregS-evoked Ca(2+) responses with an apparent IC 50 of 17.1 μmol/L. Taken together, our findings demonstrate that Dic inhibits human TRPM3 without interacting with the channel pore.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.