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Updated: Jul 10, 2026

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
Tumor necrosis factor alpha enhances nicotinic receptor up-regulation via a p38MAPK-dependent pathway
Lorise C Gahring1, Amber V Osborne-Hereford, Gustavo A Vasquez-Opazo
1Salt Lake City Veterans Affairs-Geriatrics Research, Education, Clinical Center, Salt Lake City, Utah 84148, USA. Lorise.Gahring@hsc.utah.edu
Abstract:
A response by key neuronal nicotinic acetylcholine receptors (nAChRs) to sustained nicotine exposure is up-regulation. Although this unusual receptor characteristic contributes to processes ranging from aging to addiction, the normal physiologic reason for this response is unknown. We find that up-regulation of [(3)H]epibatidine binding and function in HEK293 cells stably expressing alpha4beta2-nAChR is significantly enhanced by co-application of the proinflammatory cytokine, tumor necrosis factor alpha. The mechanism of tumor necrosis factor alpha-enhanced up-regulation requires transcription, new protein synthesis, and signaling through p38(MAPK) as demonstrated by complete inhibition using SB 202190. This finding extends the possibilities for nAChR-inflammatory interactions in normal physiological processes and offers novel insights into endogenous mechanisms that can modify up-regulation.
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