Arginine vasopressin inhibits adipogenesis in human adipose-derived stem cells

• hASCs have V1a receptors and are responsive to AVP during adipogenesis.
• AVP signaling is via the Gq-PLC-IP3 pathway which increases intracellular Ca2+.
• Ca2+ influx and release by the endoplasmic reticulum are the Ca2+ sources.
• AVP inhibits adipocyte differentiation.

Intracellular Ca2+ signaling is important for stem cell differentiation and there is evidence it may coordinate the process. Arginine vasopressin (AVP) is a neuropeptide hormone secreted mostly from the posterior pituitary gland and increases Ca2+ signals mainly via V1 receptors. However, the role of AVP in adipogenesis of human adipose-derived stem cells (hASCs) is unknown. In this study, we identified the V1a receptor gene in hASCs and demonstrated that AVP stimulation increased intracellular Ca2+ concentration during adipogenesis. This effect was mediated via V1a receptors, Gq-proteins and the PLC-IP3 pathway. These Ca2+ signals were due to endoplasmic reticulum release and influx from the extracellular space. Furthermore, AVP supplementation to the adipogenic medium decreased the number of adipocytes and adipocyte marker genes during differentiation. The effect of AVP on adipocyte formation was reversed by the V1a receptor blocker V2255. These findings suggested that AVP may function to inhibit adipocyte differentiation.