Title : Naltrexone Restores Impaired Transient Receptor Potential Melastatin 3 Ion Channel Function in Natural Killer Cells From Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients.

Pub. Date : 2019

PMID : 31736966






8 Functional Relationships(s)
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1 Naltrexone Restores Impaired Transient Receptor Potential Melastatin 3 Ion Channel Function in Natural Killer Cells From Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients. Naltrexone transient receptor potential cation channel subfamily M member 3 Homo sapiens
2 Naltrexone hydrochloride (NTX) acts as an antagonist to the muOR thus negating the inhibitory function of this opioid receptor on TRPM3. Naltrexone transient receptor potential cation channel subfamily M member 3 Homo sapiens
3 Naltrexone hydrochloride (NTX) acts as an antagonist to the muOR thus negating the inhibitory function of this opioid receptor on TRPM3. Naltrexone transient receptor potential cation channel subfamily M member 3 Homo sapiens
4 Therefore, understanding the mechanism of action for NTX in regulating and modulating TRPM3 channel function in NK cells will provide important information for the development of effective therapeutic interventions for ME/CFS. Naltrexone transient receptor potential cation channel subfamily M member 3 Homo sapiens
5 Importantly, TRPM3 channel activity was restored in IL-2 stimulated NK cells isolated from ME/CFS patients after incubation for 24 h with NTX. Naltrexone transient receptor potential cation channel subfamily M member 3 Homo sapiens
6 Moreover, we demonstrated that NTX does not act as an agonist by directly coupling on the TRPM3 ion channel gating. Naltrexone transient receptor potential cation channel subfamily M member 3 Homo sapiens
7 The opioid antagonist NTX has the potential to negate the inhibitory function of opioid receptors on TRPM3 in NK cells from ME/CFS patients, resulting in calcium signals remodeling, which will in turn affect cell functions, supporting the hypothesis that NTX may have potential for use as a treatment for ME/CFS. Naltrexone transient receptor potential cation channel subfamily M member 3 Homo sapiens
8 The opioid antagonist NTX has the potential to negate the inhibitory function of opioid receptors on TRPM3 in NK cells from ME/CFS patients, resulting in calcium signals remodeling, which will in turn affect cell functions, supporting the hypothesis that NTX may have potential for use as a treatment for ME/CFS. Naltrexone transient receptor potential cation channel subfamily M member 3 Homo sapiens