Effects mediated by the ?7 nicotinic acetylcholine receptor on cell proliferation and migration in rat adipose-derived stem cells

Adipose-derived stem cells (ASCs) are an attractive source for regenerative medicine as they can be easily iso-lated, rapidly expandable in culture and show excellent in vitro differentiation potential. Acetylcholine (ACh), one of the main neurotransmitters in central and peripheral nervous systems, plays key roles in the control of several physiological processes also in non-neural tissues. As demonstrated in our previous studies, ACh can contribute to the rat ASCs physiology, negatively modulating ASCs proliferation and migration via M2 mus-carinic receptor (mAChR) activation. In the present work we show that rat ASCs also express ?7 nicotinic receptors (nAChRs). In particular, we have investigated the effects mediated by the selective activation of ?7 nAChRs, which causes a reduction of ASC proliferation without affecting cell survival and morphology, and significantly promotes cell migration via upregulation of the CXCR4 expression. Interestingly, the activation of the ?7 nAChR also upregulates the expression of M2 mAChR protein, indicating a cooperation between muscarinic and nicotinic receptors in the inhibition of ASC proliferation.