دورية أكاديمية
أعرض في EDS

RgIA4 Prevention of Acute Oxaliplatin-Induced Cold Allodynia Requires α9-Containing Nicotinic Acetylcholine Receptors and CD3 + T-Cells.

التفاصيل البيبلوغرافية
العنوان: RgIA4 Prevention of Acute Oxaliplatin-Induced Cold Allodynia Requires α9-Containing Nicotinic Acetylcholine Receptors and CD3 + T-Cells.
المؤلفون: Huynh PN; School of Biological Sciences, University of Utah, Salt Lake City, UT 84112, USA., Christensen SB; School of Biological Sciences, University of Utah, Salt Lake City, UT 84112, USA., McIntosh JM; School of Biological Sciences, University of Utah, Salt Lake City, UT 84112, USA.; George E. Wahlen Veterans Affairs Medical Center, Salt Lake City, UT 84112, USA.; Department of Psychiatry, University of Utah, Salt Lake City, UT 84112, USA.
المصدر: Cells [Cells] 2022 Nov 11; Vol. 11 (22). Date of Electronic Publication: 2022 Nov 11.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101600052 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4409 (Electronic) Linking ISSN: 20734409 NLM ISO Abbreviation: Cells Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI
مواضيع طبية MeSH: Receptors, Nicotinic* , Neuralgia*/chemically induced , Neuralgia*/drug therapy , Drug-Related Side Effects and Adverse Reactions*, Animals ; Mice ; Oxaliplatin/adverse effects ; Hyperalgesia/chemically induced ; Hyperalgesia/drug therapy
مستخلص: Chemotherapy-induced neuropathic pain is a debilitating and dose-limiting side effect. Oxaliplatin is a third-generation platinum and antineoplastic compound that is commonly used to treat colorectal cancer and commonly yields neuropathic side effects. Available drugs such as duloxetine provide only modest benefits against oxaliplatin-induced neuropathy. A particularly disruptive symptom of oxaliplatin is painful cold sensitivity, known as cold allodynia. Previous studies of the Conus regius peptide, RgIA, and its analogs have demonstrated relief from oxaliplatin-induced cold allodynia, yielding improvement that persists even after treatment cessation. Moreover, underlying inflammatory and neuronal protection were shown at the cellular level in chronic constriction nerve injury models, consistent with disease-modifying effects. Despite these promising preclinical outcomes, the underlying molecular mechanism of action of RgIA4 remains an area of active investigation. This study aimed to determine the necessity of the α9 nAChR subunit and potential T-cell mechanisms in RgIA4 efficacy against acute oxaliplatin-induced cold allodynia. A single dose of oxaliplatin (10 mg/kg) was utilized followed by four daily doses of RgIA4. Subcutaneous administration of RgIA4 (40 µg/kg) prevented cold allodynia in wildtype mice but not in mice lacking the α9 nAChR-encoding gene, chrna9 . RgIA4 also failed to reverse allodynia in mice depleted of CD3 + T-cells. In wildtype mice treated with oxaliplatin, quantitated circulating T-cells remained unaffected by RgIA4. Together, these results show that RgIA4 requires both chrna9 and CD3 + T-cells to exert its protective effects against acute cold-allodynia produced by oxaliplatin.
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معلومات مُعتمدة: R35 GM136430 United States GM NIGMS NIH HHS
فهرسة مساهمة: Keywords: T-cells; analgesia; cold allodynia; nAChR; non-opioid; α9-containing
المشرفين على المادة: 04ZR38536J (Oxaliplatin)
0 (Receptors, Nicotinic)
تواريخ الأحداث: Date Created: 20221126 Date Completed: 20221129 Latest Revision: 20230115
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC9688540
DOI: 10.3390/cells11223561
PMID: 36428990
قاعدة البيانات: MEDLINE
الوصف
تدمد:2073-4409
DOI:10.3390/cells11223561