Angiotensin II stimulates melanogenesis via the protein kinase C pathway.

Melanogenesis is a physiological process that results in the synthesis of melanin pigments, which serve a crucial function in hyperpigmentation. The aim of the present study was to determine the effects of angiotensin II (Ang II) on melanogenesis and to elucidate the molecular events of Ang II-induced melanogenesis. Experiments were performed on human melanocytes to elucidate the pigmenting effect of Ang II and the underlying mechanisms. The elements involved in melanogenesis, including melanin content, tyrosinase (TYR) activity, and microphthalmia-associated transcription factor (MITF) and TYR expression at the mRNA and protein levels were evaluated. Melanin content and TYR activity increased in response to Ang II treatment in a concentration-dependent manner. MITF and TYR mRNA and protein expression levels were increased significantly in response to Ang II in a concentration-dependent manner. The Ang II-induced increase in melanin synthesis was reduced significantly in response to co-treatment with Ro-32-0432, a protein kinase C (PKC) inhibitor, whereas co-treatment with H-89, a PKA inhibitor, did not attenuate the Ang II-induced increase in melanin levels. These results suggest that PKC is required for Ang II-induced pigmentation in human melanocytes and that the mechanism involves the PKC pathway and MITF upregulation.

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

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 concentration­dependent 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.