Molecular Mechanisms of the Inhibitory Effects of Bovine Lactoferrin on Lipopolysaccharide-mediated Osteoclastogenesis

Inubushi, Toshihiro; Kawazoe, Aki; Miyauchi, Mutsumi; Kudo, Yasusei; Ao, Min; Ishikado, Atsushi; Makino, Tomoki; Takata, Takashi

doi:10.1074/jbc.m111.324673

Cited by 58 publications

(63 citation statements)

References 39 publications

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“…The present study's immunohistochemical findings also revealed that orally administered LbLF markedly downregulated LPS‐induced TNF‐α immunolocalization in the PDL, mainly in the alveolar crest. In a previous study, we have shown that bLF inhibited TRAF6‐dependent activation of the NF‐κB signaling pathway in osteoblasts 16 . Notably, it was demonstrated that internalized bLF binds to TRAF6, resulting in the inhibition of TRAF6‐mediating signaling pathway.…”

Section: Discussionmentioning

confidence: 88%

“…Recently, we reported that orally administered liposomal bLF (LbLF) inhibits LPS‐induced periodontal tissue breakdown in rats by suppressing TNF‐α production from cells of the periodontal tissue 15 . Notably, we demonstrated that bLF impairs LPS‐mediated TNF‐α and receptor activator of nuclear factor‐κB (NF‐κB) ligand (RANKL) production by inhibiting NF‐κB activation through interaction with TNF receptor‐associated factor 6 (TRAF6) 16 . In addition, a human trial of LbLF supplementation showed the efficacy of this treatment for periodontal disease 17 .…”

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confidence: 99%

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Orally Administered Liposomal Lactoferrin Inhibits Inflammation‐Related Bone Breakdown Without Interrupting Orthodontic Tooth Movement

Kawazoe

Inubushi

Miyauchi

et al. 2013

Journal of Periodontology

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Section: Discussionmentioning

confidence: 88%

mentioning

confidence: 99%

Orally Administered Liposomal Lactoferrin Inhibits Inflammation‐Related Bone Breakdown Without Interrupting Orthodontic Tooth Movement

Kawazoe

Inubushi

Miyauchi

et al. 2013

Journal of Periodontology

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“…Focusing on cell behavior in response to LF and HA, the three conjugates with different amounts of protein attached onto HA nanocrystals, HA–LF (a), HA–LF (b), and HA–LF (c), were initially evaluated. Moreover, physiological concentration of LF (10 µg mL −1 ) that has recently showed in vivo to have a role in bone growth, healing and a potential therapeutic role as an anabolic factor in osteoporosis was also tested . The results showed no differences in cell proliferation among all the groups for the first 4 days of culture.…”

Section: Discussionmentioning

confidence: 99%

Effect of hydroxyapatite nanocrystals functionalized with lactoferrin in osteogenic differentiation of mesenchymal stem cells

Montesi

Panseri

Iafisco

et al. 2014

J. Biomed. Mater. Res.

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Lactoferrin (LF) is a bioactive glycoprotein that became recently interesting in the field of bone regeneration for its modulatory effect on bone cells. On the basis of this evidence this work aims to functionalize biomimetic hydroxyapatite (HA) nanocrystals with LF to study their effect on osteogenic differentiation of mesenchymal stem cells (MSCs). The orientation of LF on the HA surface was analyzed by spectroscopic and thermal techniques. Three samples with different amounts of LF attached to HA nanocrystals were tested in vitro. The combined effect of HA and LF on MSC proliferation and morphology, alkaline phosphatase (ALP) activity, and gene expression were evaluated at different time points. The sample with the lowest LF amount showed the best bioactivity probably due to the formation of a single layer of protein with a better molecular orientation. Coupling of HA-LF did not affect cell proliferation and morphology, while analysis of HA-LF on ALP activity and messenger RNA expression of the selected genes, demonstrated the role of HA-LF in the induction of osteogenic markers. HA-LF represents a promising system to be used to manufacture bioactive functional materials in tissue engineering (as scaffolds, injectable cements, or coatings for metallic implants) with enhanced anabolic activity to treat bone diseases.

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“…For instance, lactoferrin inhibits lipopolysaccharide-induced DNA-binding activity of NF-κB, as well as IκBα and IKKβ phosphorylation [22]. We hypothesized that the inhibition of colitis-associated colorectal dysplasia by lactoferrin in mice may be related to its anti-inflammatory function.…”

Section: Resultsmentioning

confidence: 99%

Lactoferrin Deficiency Promotes Colitis-Associated Colorectal Dysplasia in Mice

Zheng

Fan

et al. 2014

PLoS ONE

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Nonresolving inflammatory processes affect all stages of carcinogenesis. Lactoferrin, a member of the transferrin family, is involved in the innate immune response and anti-inflammatory, anti-microbial, and anti-tumor activities. We previously found that lactoferrin is significantly down-regulated in specimens of nasopharyngeal carcinoma (NPC) and negatively associated with tumor progression, metastasis, and prognosis of patients with NPC. Additionally, lactoferrin expression levels are decreased in colorectal cancer as compared with normal tissue. Lactoferrin levels are also increased in the various phases of inflammation and dysplasia in an azoxymethane–dextran sulfate sodium (AOM-DSS) model of colitis-associated colon cancer (CAC). We thus hypothesized that the anti-inflammatory function of lactoferrin may contribute to its anti-tumor activity. Here we generated a new Lactoferrin knockout mouse model in which the mice are fertile, develop normally, and display no gross morphological abnormalities. We then challenged these mice with chemically induced intestinal inflammation to investigate the role of lactoferrin in inflammation and cancer development. Lactoferrin knockout mice demonstrated a great susceptibility to inflammation-induced colorectal dysplasia, and this characteristic may be related to inhibition of NF-κB and AKT/mTOR signaling as well as regulation of cell apoptosis and proliferation. Our results suggest that the protective roles of lactoferrin in colorectal mucosal immunity and inflammation-related malignant transformation, along with a deficiency in certain components of the innate immune system, may lead to serious consequences under conditions of inflammatory insult.

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Molecular Mechanisms of the Inhibitory Effects of Bovine Lactoferrin on Lipopolysaccharide-mediated Osteoclastogenesis

Cited by 58 publications

References 39 publications

Orally Administered Liposomal Lactoferrin Inhibits Inflammation‐Related Bone Breakdown Without Interrupting Orthodontic Tooth Movement

Orally Administered Liposomal Lactoferrin Inhibits Inflammation‐Related Bone Breakdown Without Interrupting Orthodontic Tooth Movement

Effect of hydroxyapatite nanocrystals functionalized with lactoferrin in osteogenic differentiation of mesenchymal stem cells

Lactoferrin Deficiency Promotes Colitis-Associated Colorectal Dysplasia in Mice

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