Hinokitiol increases the angiogenic potential of dental pulp cells through ERK and p38MAPK activation and hypoxia-inducible factor-1α (HIF-1α) upregulation |
| |
| Institution: | 1. Department of Oral Physiology, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea;2. Department of Dental Pharmacology, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea;3. Department of Oral and Maxillofacial Surgery, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea;4. Department of Oral Pathology, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea;5. Department of Oral and Maxillofacial Pathobiology, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima 734-8553, Japan;1. Department of Pediatric Dentistry, School of Dentistry, Federal University of Rio Grande do Sul, Porto Alegre, Brazil;2. School of Pharmacy, Federal University of Rio Grande do Sul, Porto Alegre, Brazil;3. Hematology and Stem Cell Laboratory, Faculty of Pharmacy, Federal University of Rio Grande do Sul, and Stem Cell Research Institute, Porto Alegre, Brazil;1. Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea;2. Translational Research Center for Protein Function Control, Yonsei University, Seoul, South Korea |
| |
| Abstract: | Hinokitiol, a natural iron-chelating agent, is known to have diverse biological and pharmacological activities in various cell types. However, the effect of hinokitiol on dental pulp cells has not yet been reported. In this study, hinokitiol increases hypoxia-inducible factor-1α (HIF-1α) protein levels and vascular endothelial growth factor (VEGF) secretion in human dental pulp cells. The extracellular-signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) pathways are involved in hinokitiol-induced HIF-1α protein expression in dental pulp cells. Conditioned media from hinokitiol-treated pulp cells enhances angiogenesis in vitro and in vivo. Overall, these results show that hinokitiol promotes ERK and p38MAPK activation and HIF-1α-induced VEGF production, thus increasing the angiogenic potential of dental pulp cells. |
| |
| Keywords: | Angiogenesis Dental pulp cells Hinokitiol Hypoxia-inducible factor-1 alpha |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
