Gingipains promote RANKL-induced osteoclastogenesis through the enhancement of integrin β3 in RAW264.7 cells

Mo, Weiyan; Luo, Haoyuan; Wu, Juan; Xu, Na; Zhang, Fuping; Qiu, Qingtao; Zhu, Wenjun; Liang, Min

doi:10.1007/s10735-020-09865-w

Cited by 6 publications

(5 citation statements)

References 33 publications

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“…During this adhesion process, FAK and paxillin phosphorylation and activity increases, indicating active mechanotransduction between focal adhesion structures and the cytoskeleton. Taken together, gingipains promote MT cascades in the context of alveolar bone resorption by both facilitating osteoclast differentiation and integrin-dependent resorption pit formation [261]. It remains to be elucidated how the presence of gingipains exactly augments the function of RANK-L. Secreted proteases, so-called gingipains (GPs), from the microbe Porphyromonas gingivalis (P. gingivalis) interact with the receptor activator of nuclear factor kappa-B ligand (RANK-L), osteoprotegerin (OPG), and receptor activator of nuclear factor kappa-B (RANK) system of osteocytes and osteoclasts.…”

Section: Porphyromonas Gingivalis-derived Proteases: a "Heavy Load" For The Periodontiummentioning

confidence: 93%

“…Gingipain-related ECM degradation is, however, not limited to fibrous components, as these proteases, in conjunction with the receptor activator of nuclear factor kappa-B ligand (RANK-L), promote osteoclastogenesis, which is a prerequisite for the destruction of the mineral matrix during alveolar bone resorption in periodontitis [261]. In detail, gingipains induce osteoclast-specific genes, such as cathepsin K, MMP-9, and alkaline phosphatase type 5, in a dose-dependent manner [262].…”

Section: Porphyromonas Gingivalis-derived Proteases: a "Heavy Load" For The Periodontiummentioning

confidence: 99%

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From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues

et al. 2021

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Among oral tissues, the periodontium is permanently subjected to mechanical forces resulting from chewing, mastication, or orthodontic appliances. Molecularly, these movements induce a series of subsequent signaling processes, which are embedded in the biological concept of cellular mechanotransduction (MT). Cell and tissue structures, ranging from the extracellular matrix (ECM) to the plasma membrane, the cytosol and the nucleus, are involved in MT. Dysregulation of the diverse, fine-tuned interaction of molecular players responsible for transmitting biophysical environmental information into the cell’s inner milieu can lead to and promote serious diseases, such as periodontitis or oral squamous cell carcinoma (OSCC). Therefore, periodontal integrity and regeneration is highly dependent on the proper integration and regulation of mechanobiological signals in the context of cell behavior. Recent experimental findings have increased the understanding of classical cellular mechanosensing mechanisms by both integrating exogenic factors such as bacterial gingipain proteases and newly discovered cell-inherent functions of mechanoresponsive co-transcriptional regulators such as the Yes-associated protein 1 (YAP1) or the nuclear cytoskeleton. Regarding periodontal MT research, this review offers insights into the current trends and open aspects. Concerning oral regenerative medicine or weakening of periodontal tissue diseases, perspectives on future applications of mechanobiological principles are discussed.

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Section: Porphyromonas Gingivalis-derived Proteases: a "Heavy Load" For The Periodontiummentioning

confidence: 93%

Section: Porphyromonas Gingivalis-derived Proteases: a "Heavy Load" For The Periodontiummentioning

confidence: 99%

From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues

et al. 2021

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“…Gingipain proteases produce effects on fibrinogen that increases the risk of periodontal bleeding in patients with periodontitis ( Haditsch et al., 2020 ; Kadowaki, 2021 ). Studies also found that the enzymes interfered coagulation through interacting with fibrinogen, prothrombin ( Imamura et al., 2001 ) and the stimulation of the kallikrein/kinin pathway ( Hočevar et al., 2018 ; Mo et al., 2020 ). Furthermore, amyloid fibrin (ogen) protein structure was observed in platelet poor plasma clots, and samples from PD patients contain much more amyloid-specific signal compared with the control donors ( Adams et al., 2019 ).…”

Section: Effects Of Bacterial Infection On Pd Pathogenesismentioning

confidence: 99%

Insights into the roles of bacterial infection and antibiotics in Parkinson’s disease

Sheng

Zhao

Zhang

2022

Front. Cell. Infect. Microbiol.

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Parkinson’s disease (PD) is one of the most common neurodegenerative disorders, which is accompanied with the classical motor symptoms and a range of non-motor symptoms. Bacterial infection affects the neuroinflammation associated with the pathology of PD and various antibiotics have also been confirmed to play an important role not only in bacterial infection, but also in the PD progression. This mini-review summarized the role of common bacterial infection in PD and introduced several antibiotics that had anti-PD effects.

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“…P. gingivalis increases the osteoclastogenic potential of OC precursors both locally and systemically [ 49 ]. In addition to LPS-mediated TLR activation, P. gingivalis releases gingipains, cysteine proteases that can induce osteoclastogenesis of RANKL-treated OCs and enhance OC activity through an increase in integrin αvβ3 and degradation of OPG in co-culture with OBs [ 50 , 51 ]. Phosphoglycerol dihydroceramide, a distinctive ceramide of P. gingivalis , has also been found to promote RANKL-induced osteoclastogenesis.…”

Section: The Infectious Milieu a Noxious Brew Of Pathogen- And Homentioning

confidence: 99%

Multitasking by the OC Lineage during Bone Infection: Bone Resorption, Immune Modulation, and Microbial Niche

Roper

Shao

Veis

2020

Cells

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Bone infections, also known as infectious osteomyelitis, are accompanied by significant inflammation, osteolysis, and necrosis. Osteoclasts (OCs) are the bone-resorbing cells that work in concert with osteoblasts and osteocytes to properly maintain skeletal health and are well known to respond to inflammation by increasing their resorptive activity. OCs have typically been viewed merely as effectors of pathologic bone resorption, but recent evidence suggests they may play an active role in the progression of infections through direct effects on pathogens and via the immune system. This review discusses the host- and pathogen-derived factors involved in the in generation of OCs during infection, the crosstalk between OCs and immune cells, and the role of OC lineage cells in the growth and survival of pathogens, and highlights unanswered questions in the field.

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Gingipains promote RANKL-induced osteoclastogenesis through the enhancement of integrin β3 in RAW264.7 cells

Cited by 6 publications

References 33 publications

From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues

From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues

Insights into the roles of bacterial infection and antibiotics in Parkinson’s disease

Multitasking by the OC Lineage during Bone Infection: Bone Resorption, Immune Modulation, and Microbial Niche

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