Cabaço Luís C, Bento-Lopes Liliana, Neto Matilde V, Ferreira Andreia, Staubli Wanja B L, Ramalho José S, Seabra Miguel C, Barral Duarte C
iNOVA4Health, NOVA Medical School, Faculdade de Ciências Médicas, NMS, FCM, Universidade NOVA de Lisboa, Lisboa, Portugal.
JID Innov. 2022 Jun 21;2(5):100139. doi: 10.1016/j.xjidi.2022.100139. eCollection 2022 Sep.
Skin pigmentation is imparted by melanin and is crucial for photoprotection against UVR. Melanin is synthesized and packaged into melanosomes within melanocytes and is then transferred to keratinocytes (KCs). Although the molecular players involved in melanogenesis have been extensively studied, those underlying melanin transfer remain unclear. Previously, our group proposed that coupled exocytosis/phagocytosis is the predominant mechanism of melanin transfer in human skin and showed an essential role for RAB11B and the exocyst tethering complex in this process. In this study, we show that soluble factors present in KC-conditioned medium stimulate melanin exocytosis from melanocytes and transfer to KCs. Moreover, we found that these factors are released by differentiated KCs but not by basal layer KCs. Furthermore, we found that RAB3A regulates melanin exocytosis and transfer stimulated by KC-conditioned medium. Indeed, KC-conditioned medium enhances the recruitment of RAB3A to melanosomes in melanocyte dendrites. Therefore, our results suggest the existence of two distinct routes of melanin exocytosis: a basal route controlled by RAB11B and a RAB3A-dependent route, stimulated by KC-conditioned medium. Thus, this study provides evidence that soluble factors released by differentiated KCs control skin pigmentation by promoting the accumulation of RAB3A-positive melanosomes in melanocyte dendrites and their release and subsequent transfer to KCs.
皮肤色素沉着由黑色素赋予,对抵御紫外线辐射的光保护至关重要。黑色素在黑素细胞内合成并包装到黑素小体中,然后转移至角质形成细胞(KC)。尽管参与黑色素生成的分子机制已得到广泛研究,但黑色素转移的潜在机制仍不清楚。此前,我们团队提出胞吐作用/吞噬作用偶联是人类皮肤中黑色素转移的主要机制,并表明RAB11B和外被体拴系复合体在此过程中起重要作用。在本研究中,我们发现KC条件培养基中存在的可溶性因子可刺激黑素细胞的黑色素胞吐作用并转移至KC。此外,我们发现这些因子由分化的KC释放,而不是由基底层KC释放。此外,我们发现RAB3A调节KC条件培养基刺激的黑色素胞吐作用和转移。实际上,KC条件培养基增强了RAB3A向黑素细胞树突中黑素小体的募集。因此,我们的结果表明存在两种不同的黑色素胞吐途径:一种由RAB11B控制的基础途径和一种由KC条件培养基刺激的依赖RAB3A的途径。因此,本研究提供了证据,表明分化的KC释放的可溶性因子通过促进RAB3A阳性黑素小体在黑素细胞树突中的积累及其释放并随后转移至KC来控制皮肤色素沉着。