Human SCs were treated with M2 selective agonist arecaidine propargyl ester hydrobromide (APE, A140; Sigma-Aldrich) at the final concentration ranging from 25 to 100 µM. Albeit APE was reported as preferential M1–M4 agonist [25 (link)], several modifications of the molecule suggested a preferential agonistic effect on M2 receptor subtype [26 (link),27 (link)]. Our works have been focused on the characterization of APE hydrobromide by pharmacological competition studies with M2 antagonists methoctramine or gallamine [8 (link),17 (link),32 (link)]. Moreover, the silencing of M2 receptors by siRNAs have largely demonstrated the selectivity of APE for M2 receptor in several cell lines (i.e., human glioblastoma, neuroblastoma, and urothelial bladder cell lines [16 (link),29 (link),30 (link),31 (link),33 (link)].
To study all muscarinic receptors activation, hSCs were treated with the non-selective muscarinic agonist, muscarine (Sigma-Aldrich), at the final concentration ranging from 25 to 100 µM.
All experiments were performed in technical and experimental triplicate.
To study all muscarinic receptors activation, hSCs were treated with the non-selective muscarinic agonist, muscarine (Sigma-Aldrich), at the final concentration ranging from 25 to 100 µM.
All experiments were performed in technical and experimental triplicate.
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