Angiotensin II promotes melanogenesis via angiotensin II type 1 receptors in human melanocytes

Abstract

Angiotensin II (AngII) is a hormone with long-established cardiovascular actions. Previous studies have revealed an additional role for AngII in the regulation of cutaneous wound healing. To evaluate the association between AngII and abnormal pigmentation of cutaneous wound healing, the present study used human melanocytes to investigate the effects of AngII on melanogenesis, and to elucidate the possible underlying mechanisms. Primary culture melanocytes were treated with AngII either alone or in combination with an AngII type 1 (AT1) receptor antagonist, losartan (LOS). The melanin content and tyrosinase activity were measured and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting were performed to assess the proteins involved in melanogenesis and the AT1 receptor. AngII regulated the mRNA expression of AT1 in the melanocytes. The melanin content and tyrosinase activity increased in response to treatment with AngII in a concentration-dependent manner. RT-qPCR and western blotting revealed that the AT1 receptor antagonist, LOS, eliminated this effect. These results provide a novel insight into the role of AngII and its associated signaling in melanogenesis.