Abstract
BackgroundPigmentation is one of the essential defense mechanisms against oxidative stress or UV irradiation; however, abnormal hyperpigmentation in human skin may pose a serious aesthetic problem. C-phycocyanin (Cpc) is a phycobiliprotein from spirulina and functions as an antioxidant and a light harvesting protein. Though it is known that spirulina has been used to reduce hyperpigmentation, little literature addresses the antimelanogenic mechanism of Cpc. Herein, we investigated the rationale for the Cpc-induced inhibitory mechanism on melanin synthesis in B16F10 melanoma cells.MethodsCpc-induced inhibitory effects on melanin synthesis and tyrosinase expression were evaluated. The activity of MAPK pathways-associated molecules such as MAPK/ERK and p38 MAPK, were also examined to explore Cpc-induced antimelanogenic mechanisms. Additionally, the intracellular localization of Cpc was investigated by confocal microscopic analysis to observe the migration of Cpc.ResultsCpc significantly (P < 0.05) reduced both tyrosinase activity and melanin production in a dose-dependent manner. This phycobiliprotein elevated the abundance of intracellular cAMP leading to the promotion of downstream ERK1/2 phosphorylation and the subsequent MITF (the transcription factor of tyrosinase) degradation. Further, Cpc also suppressed the activation of p38 causing the consequent disturbed activation of CREB (the transcription factor of MITF). As a result, Cpc negatively regulated tyrosinase gene expression resulting in the suppression of melanin synthesis. Moreover, the entry of Cpc into B16F10 cells was revealed by confocal immunofluorescence localization and immunoblot analysis.ConclusionsCpc exerted dual antimelanogenic mechanisms by upregulation of MAPK/ERK-dependent degradation of MITF and downregulation of p38 MAPK-regulated CREB activation to modulate melanin formation. Cpc may have potential applications in biomedicine, food, and cosmetic industries.
Highlights
Pigmentation is one of the essential defense mechanisms against oxidative stress or UV irradiation; abnormal hyperpigmentation in human skin may pose a serious aesthetic problem
The exalted phosphorylation of extracellular signal-regulated protein kinases (ERKs) activates the transcription factors such as c-myc and c-fos. This phosphorylation may lead to the degradation of microphthalmia-associated transcription factor (MITF), a transcription factor associated with cell development, survival and certain activities
We evaluated the potential of Cpc to be used as an antimelanogenic agent and explored the involvement of ERK and p38 mitogen-activated protein kinases (MAPK) in Cpc-induced antimelanogenic regulation in B16F10 melanoma cells
Summary
Pigmentation is one of the essential defense mechanisms against oxidative stress or UV irradiation; abnormal hyperpigmentation in human skin may pose a serious aesthetic problem. C-phycocyanin (Cpc), a major type of phycocyanin of phycobilisome in spirulina, has been suggested to exhibit radical-scavenging property [1] to reduce inflammatory responses [2,3] and oxidative stress [1,4]. This phycobiliprotein induces HeLa cell apoptosis [5,6] enhances. It is suggested that Cpc regulates the mitogen-activated protein kinases (MAPK) pathways, such as p38 MAPK, and extracellular signal-regulated protein kinases (ERKs) These signaling are known to respond to extracellular stress stimuli to regulate several cellular activities including proliferation, survival/apoptosis, gene expression, and differentiation. MITF is critical in transcriptional activation of genes required for melanogenesis (tyrosinase, TYRP1, and TYRP2), survival, as well as the differentiation of melanocytes [18]
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