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Title: HMGB1 promotes intraoral palatal wound 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
Mahidol University
Hokkaido University
Kagoshima University
Kurume University School of Medicine
Department of Anesthesiology and Intensive Care
Keywords: Biochemistry, Genetics and Molecular Biology;Chemical Engineering;Chemistry;Computer Science
Issue Date: 23-Nov-2016
Citation: International Journal of Molecular Sciences. Vol.17, No.11 (2016)
Abstract: © 2016 by the authors; licensee MDPI, Basel, Switzerland. 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 (Hmgb1+/−) mice and Wild-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 Hmgb1+/−and WT mice on Day 3 after wounding. Mallory Azan staining showed densely packed of collagen fibers in WT mice, whereas in Hmgb1+/−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 Hmgb1+/−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.
ISSN: 14220067
Appears in Collections:Scopus 2016-2017

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