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Semaxanib, a VEGF inhibitor, suppresses melanogenesis by modulating CRTC3 independently of VEGF signaling.
Kwon, HyeJi; Lee, Jeong Hyeon; Yoo, Jae Min; Nguyen, Huonggiang; An, Hongchan; Chang, Sung Eun; Song, Youngsup.
Afiliación
  • Kwon H; Department of Brain Sciences, Brain Korea 21 project, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
  • Lee JH; Department of Dermatology, Brain Korea 21 project, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
  • Yoo JM; Department of Dermatology, Brain Korea 21 project, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
  • Nguyen H; Department of Brain Sciences, Brain Korea 21 project, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
  • An H; College of Pharmacy and Insitute of Pharmaceutical Sciences, CHA University Pocheon, Gyeonggi-do, Korea. Electronic address: hongchanan@cha.ac.kr.
  • Chang SE; Department of Dermatology, Brain Korea 21 project, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea. Electronic address: cse@amc.seoul.kr.
  • Song Y; Department of Brain Sciences, Brain Korea 21 project, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea. Electronic address: ysong@amc.seoul.kr.
J Dermatol Sci ; 115(3): 121-129, 2024 Sep.
Article en En | MEDLINE | ID: mdl-39127591
ABSTRACT

BACKGROUND:

Dysregulation of melanogenesis contributes to the development of skin hyperpigmentation diseases, which poses a treatment challenge. Following the establishment of CRTC3 screening methods to explore small molecules inhibiting melanogenesis for the topical treatment of hyperpigmentation diseases, we identified a candidate molecule, semaxanib.

OBJECTIVE:

To explore the antimelanogenic effects of semaxanib, a vascular endothelial growth factor receptor (VEGFR) 2 inhibitor, for potential applications in hyperpigmentation management and to unravel the role of VEGF signaling in melanocyte biology by investigating mechanism of action of semaxanib.

METHODS:

Mouse-derived spontaneously immortalized melanocytes, B16F10, and normal human primary epidermal melanocytes cells were treated with semaxanib, and cellular responses were assessed using cell viability assays and melanin content measurements. Molecular mechanisms were investigated using transcriptional activity assays, reverse-transcription polymerase chain reaction, and immunoblotting analysis. In vivo studies were conducted using an epidermis-humanized transgenic mouse model and ex vivo human skin tissues.

RESULTS:

Semaxanib ameliorated melanin content in cultured melanocytes by downregulating the expression of melanogenesis-associated genes by suppressing the CRTC3/microphthalmia-associated transcription factors. Topical application of semaxanib reduced melanin accumulation in the ultraviolet B-stimulated ex vivo human epidermis and tail of K14-stem cell factor transgenic mice. Mechanistically, the antimelanogenic effect induced by semaxanib was associated with SIK2-CRTC3-MITF rather than VEGF signaling in melanocytes.

CONCLUSION:

Semaxanib emerges as a promising candidate for the development of therapeutics for hyperpigmentation, potentially working independently of VEGF signaling in human melanocytes.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factores de Transcripción / Transducción de Señal / Factor A de Crecimiento Endotelial Vascular / Factor de Transcripción Asociado a Microftalmía / Melaninas / Melanocitos Límite: Animals / Humans Idioma: En Revista: J Dermatol Sci Asunto de la revista: DERMATOLOGIA Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factores de Transcripción / Transducción de Señal / Factor A de Crecimiento Endotelial Vascular / Factor de Transcripción Asociado a Microftalmía / Melaninas / Melanocitos Límite: Animals / Humans Idioma: En Revista: J Dermatol Sci Asunto de la revista: DERMATOLOGIA Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos