Rational Design of a Modality-Specific Inhibitor of TRPM8 Channel against Oxaliplatin-Induced Cold Allodynia.
Aerziguli AierkenYa-Kai XieWenqi DongAbuliken ApaerJia-Jia LinZihan ZhaoShilong YangZhen-Zhong XuFan YangPublished in: Advanced science (Weinheim, Baden-Wurttemberg, Germany) (2021)
Platinum-based compounds in chemotherapy such as oxaliplatin often induce peripheral neuropathy and neuropathic pain such as cold allodynia in patients. Transient Receptor Potential Melastatin 8 (TRPM8) ion channel is a nociceptor critically involved in such pathological processes. Direct blockade of TRPM8 exhibits significant analgesic effects but also incurs severe side effects such as hypothermia. To selectively target TRPM8 channels against cold allodynia, a cyclic peptide DeC-1.2 is de novo designed with the optimized hot-spot centric approach. DeC-1.2 modality specifically inhibited the ligand activation of TRPM8 but not the cold activation as measured in single-channel patch clamp recordings. It is further demonstrated that DeC-1.2 abolishes cold allodynia in oxaliplatin treated mice without altering body temperature, indicating DeC-1.2 has the potential for further development as a novel analgesic against oxaliplatin-induced neuropathic pain.
Keyphrases
- neuropathic pain
- spinal cord
- spinal cord injury
- end stage renal disease
- newly diagnosed
- high glucose
- diabetic rats
- chronic kidney disease
- ejection fraction
- cardiac arrest
- prognostic factors
- peritoneal dialysis
- brain injury
- risk assessment
- human health
- endothelial cells
- squamous cell carcinoma
- oxidative stress
- high fat diet induced
- insulin resistance
- rectal cancer
- wild type
- cerebral ischemia