Pocket Epithelium in the Pathological Setting for HMGB1 Release

Ebe, Noriko; Miki, Hirokazu; Iwasaki, Kengo; Iseki, Sachiko; Okuhara, Shigeru; Podyma‐Inoue, Katarzyna Α.; Terasawa, Kazuya; Watanabe, Akira; T, Akizuki; Watanabe, Hirotaka; Yanagishita, Masaki; Izumi, Yuichi

doi:10.1177/0022034510385688

Cited by 28 publications

(33 citation statements)

References 33 publications

(51 reference statements)

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“…Consequently, HMGB1 may be located in the cytoplasm of epithelial cells lining the gingival crevice, which harbors mature dental plaque rich in butyrate. This hypothesis is consistent with a report that HMGB1 was present mainly in the cytoplasm of periodontal-pocket gingival epithelial cells (91). In such environments, acetylated HMGB1 in the cytoplasm can be easily released from the gingival cells by butyrate-induced autophagic cell death.…”

Section: Possible Relationship Of Cell Death To Periodontal Diseasesupporting

confidence: 93%

“…Therefore, destruction of the cell membrane may cause HMGB1 to leak from cells. In fact, Ebe et al reported that butyrate-induced death of Ca9-22 gingival epithelial cells was accompanied by necrotic features, and they concluded that dead cells may release HMGB1 (91). In sum, these studies suggest that autophagic cell death is closely related to butyrate-induced HMGB1 release.…”

Section: Possible Relationship Of Cell Death To Periodontal Diseasementioning

confidence: 91%

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Programmed cell death and its possible relationship with periodontal disease

et al. 2012

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Cell death occurs in physiological conditions and as a result of injury or disease. Programmed cell death has an important role in the development and homeostasis of human tissue. Aberrant regulation of this process is thought to cause numerous diseases, including developmental disorders, neurodegenerative disease, and cancer. Apoptosis is the main type of programmed cell death and is well understood. However, recent intensive studies have revealed other types of programmed cell death. Here, we include an overview of three types of programmed cell death: apoptosis, necroptosis, and autophagic cell death. We also provide information on damage-associated molecular patterns (DAMPs), which have proinflammatory effects and are reportedly associated with cell death. Finally, we discuss the link between programmed cell death and periodontal disease and propose a hypothetical role for programmed cell death and DAMPs-which are released from cytoplasm of necrotic cells-in periodontal disease initiation. (J Oral Sci 54, 137-149, 2012)

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Section: Possible Relationship Of Cell Death To Periodontal Diseasesupporting

confidence: 93%

Section: Possible Relationship Of Cell Death To Periodontal Diseasementioning

confidence: 91%

Programmed cell death and its possible relationship with periodontal disease

et al. 2012

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“…Many studies have shown that HMGB1 is secreted from many types of cells, including HGF (22), under stressed conditions (2,(8)(9)(10). The gingival crevicular fluid (GCF) of patients with periodontal disease contains high levels of HMGB1 (23), possibly released from inflamed epithelium in periodontal pockets (24), as well as activated immune cells (2,5). Extracellular HMGB1, apart from its cytokine activity, affects the proliferation and/or migration of many cell types (11,12,15,17,25).…”

Section: Discussionmentioning

confidence: 99%

Role of HMGB1 in proliferation and migration of human gingival and periodontal ligament fibroblasts

2013

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High mobility group box 1 (HMGB1)was originally defined as a nuclear protein. However, later studies showed that HMGB1 was released from damaged cells into the extracellular milieu and functioned as a danger signaling molecule. HMGB1 has also been shown to exert proliferative and chemoattractant effects on many cell types. In this study, we investigated the in vitro effect of human recombinant HMGB1 on the proliferation and migration of human gingival fibroblasts (HGF) and human periodontal ligament fibroblasts (HPDLF). For the proliferation assay, HGF and HPDLF were cultured in the presence of 5, 10, and 50 ng/mL HMGB1. After a period of 6 days, cell proliferation was determined by MTT assay.

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“…A cell monolayer scratch assay is used to evaluate keratinocyte proliferation and migration during re-epithelialization [31]. To assess whether delayed in the wound healing at the wound sites of the Hmgb1 +/− mice is accompanied by retarded re-epithelialization mechanism, gingival epithelial cells were subjected to wound-healing (scratch) assay, in which the ability of cells to migrate and cover the cell-free space is monitored.…”

Section: Resultsmentioning

confidence: 99%

HMGB1 Promotes Intraoral Palatal Wound Healing through RAGE-Dependent Mechanisms

Tancharoen

Gando

Shrestha

et al. 2016

IJMS

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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.

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Pocket Epithelium in the Pathological Setting for HMGB1 Release

Cited by 28 publications

References 33 publications

Programmed cell death and its possible relationship with periodontal disease

Programmed cell death and its possible relationship with periodontal disease

Role of HMGB1 in proliferation and migration of human gingival and periodontal ligament fibroblasts

HMGB1 Promotes Intraoral Palatal Wound Healing through RAGE-Dependent Mechanisms

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