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- Title
HMGB1 Promotes Intraoral PalatalWound Healing through RAGE-Dependent Mechanisms.
- Authors
Salunya Tancharoen; Satoshi Gando; Shrestha Binita; Tomoka Nagasato; Kiyoshi Kikuchi; Yuko Nawa; Pornpen Dararat; Mika Yamamoto; Somphong Narkpinit; Ikuro Maruyama
- Abstract
High mobility group box 1 (HMGB1) is tightly connected to the process of tissue organization upon tissue injury. Here we show that HMGB1 controls epithelium and connective tissue regeneration both in vivo and in vitro during palatal wound healing. Heterozygous HMGB1 (Hmgb+/-) mice andWild-type (WT) mice were subjected to palatal injury. Maxillary tissues were stained with Mallory Azan or immunostained with anti-HMGB1, anti-proliferating cell nuclear antigen (PCNA), anti-nuclear factor-κB (NF-κB) p50 and anti-vascular endothelial growth factor (VEGF) antibodies. Palatal gingival explants were cultured with recombinant HMGB1 (rHMGB1) co-treated with siRNA targeting receptor for advanced glycation end products (RAGEs) for cell migration and PCNA expression analysis. Measurement of the wound area showed differences between Hmgb+/- and WT mice on Day 3 after wounding. Mallory Azan staining showed densely packed of collagen fibers in WT mice, whereas in Hmgb+/- mice weave-like pattern of low density collagen bundles were present. At three and seven days post-surgery, PCNA, NF-κB p50 and VEGF positive keratinocytes of WT mice were greater than that of Hmgb+/- mice. Knockdown of RAGE prevents the effect of rHMGB1-induced cell migration and PCNA expression in gingival cell cultures. The data suggest that HMGB1/RAGE axis has crucial roles in palatal wound healing.
- Subjects
HIGH mobility group proteins; EPITHELIUM; WOUND healing; KERATINOCYTES; CELL culture
- Publication
International Journal of Molecular Sciences, 2016, Vol 17, Issue 11, p1961
- ISSN
1661-6596
- Publication type
Article
- DOI
10.3390/ijms17111961