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Publication : HMGB1 Promotes Intraoral Palatal Wound Healing through RAGE-Dependent Mechanisms.

First Author  Tancharoen S Year  2016
Journal  Int J Mol Sci Volume  17
Issue  11 PubMed ID  27886093
Mgi Jnum  J:313241 Mgi Id  MGI:6791848
Doi  10.3390/ijms17111961 Citation  Tancharoen S, et al. (2016) HMGB1 Promotes Intraoral Palatal Wound Healing through RAGE-Dependent Mechanisms. Int J Mol Sci 17(11):1961
abstractText  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-kappaB (NF-kappaB) 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-kappaB 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.
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