Oxidative stress induced pyroptosis leads to osteogenic dysfunction of MG63 cells

Liu, Shanshan; Du, Juan; Li, Dongfang; Yang, Panpan; Kou, Yuying; Li, Congshan; Zhou, Qin; Lu, Yupu; Hasegawa, Tomoka; Li, Minqi

doi:10.1007/s10735-020-09874-9

Cited by 51 publications

(51 citation statements)

References 46 publications

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“…38 In osteoblasts, MCC950 inhibits NLRP3 inflammasome-mediated pyroptosis and promotes early osteogenic differentiation. 39 Correspondingly, our data also found that NLRP3 KO mice had increased osteoblast activity in ligature-induced periodontitis, compared with WT mice. Thus, it is possible that the increased alveolar bone volume caused by NLRP3 deficiency may be partly due to the effects of NLRP3 on osteoblast differentiation.…”

Section: Discussionsupporting

confidence: 78%

NLRP3 regulates alveolar bone loss in ligature‐induced periodontitis by promoting osteoclastic differentiation

Chen

Yang

et al. 2020

Cell Proliferation

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Section: Discussionsupporting

confidence: 78%

NLRP3 regulates alveolar bone loss in ligature‐induced periodontitis by promoting osteoclastic differentiation

Chen

Yang

et al. 2020

Cell Proliferation

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“…Hence, increased DKK1 levels generated by osteocytes in osteolytic diseases, such as periodontitis, may also contribute to the increased activity of the NLRP3 inflammasome in these scenarios, although stronger, direct evidence is still needed ( 1 ). In addition, pyroptosis triggered by inflammasome activation can also determine the death of osteoblasts, thereby decreasing the rate of osteogenesis ( 149 ). Inhibition of NLRP3 and caspase-1 reverses the reduction in bone formation induced by pyroptosis in MC3T3-E1 cells ( 150 ).…”

Section: Mechanisms Of Bone Loss Related To Inflammasomesmentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

Ling

Jiang

2021

Front. Immunol.

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Bone remodeling is tightly controlled by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Fine tuning of the osteoclast–osteoblast balance results in strict synchronization of bone resorption and formation, which maintains structural integrity and bone tissue homeostasis; in contrast, dysregulated bone remodeling may cause pathological osteolysis, in which inflammation plays a vital role in promoting bone destruction. The alveolar bone presents high turnover rate, complex associations with the tooth and periodontium, and susceptibility to oral pathogenic insults and mechanical stress, which enhance its complexity in host defense and bone remodeling. Alveolar bone loss is also involved in systemic bone destruction and is affected by medication or systemic pathological factors. Therefore, it is essential to investigate the osteoimmunological mechanisms involved in the dysregulation of alveolar bone remodeling. The inflammasome is a supramolecular protein complex assembled in response to pattern recognition receptors and damage-associated molecular patterns, leading to the maturation and secretion of pro-inflammatory cytokines and activation of inflammatory responses. Pyroptosis downstream of inflammasome activation also facilitates the clearance of intracellular pathogens and irritants. However, inadequate or excessive activity of the inflammasome may allow for persistent infection and infection spreading or uncontrolled destruction of the alveolar bone, as commonly observed in periodontitis, periapical periodontitis, peri-implantitis, orthodontic tooth movement, medication-related osteonecrosis of the jaw, nonsterile or sterile osteomyelitis of the jaw, and osteoporosis. In this review, we present a framework for understanding the role and mechanism of canonical and noncanonical inflammasomes in the pathogenesis and development of etiologically diverse diseases associated with alveolar bone loss. Inappropriate inflammasome activation may drive alveolar osteolysis by regulating cellular players, including osteoclasts, osteoblasts, osteocytes, periodontal ligament cells, macrophages, monocytes, neutrophils, and adaptive immune cells, such as T helper 17 cells, causing increased osteoclast activity, decreased osteoblast activity, and enhanced periodontium inflammation by creating a pro-inflammatory milieu in a context- and cell type-dependent manner. We also discuss promising therapeutic strategies targeting inappropriate inflammasome activity in the treatment of alveolar bone loss. Novel strategies for inhibiting inflammasome signaling may facilitate the development of versatile drugs that carefully balance the beneficial contributions of inflammasomes to host defense.

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“…The present study demonstrated that puerarin alleviates HG-induced oxidative stress in HRECs, suggesting a potential of puerarin being applied to the treatment of DR. Pyroptosis is identified as inflammatory caspases (mainly CASP1)-dependent programmed cell death (Bergsbaken et al 2009). Accumulating evidence shows that oxidative stressinduced pyroptosis is closely related to the development of multiple diseases (Liu et al 2020;Zhou et al 2020). What's more, a recent study found that pyroptosis is involved in the progression of DR, which can be mediated by oxidative stress (Xi et al 2020).…”

Section: Discussionmentioning

confidence: 99%

Puerarin protects against human retinal endothelial cells injury induced by high glucose via regulating miR-16-5p/CASP1 axis

Zhang¹,

Chen²,

Gao³

2023

gpb

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We aimed to investigate the effects of puerarin on high glucose (HG)-induced human retinal endothelial cells (HRECs) injury. Cells were exposed to puerarin in the presence or absence of HG challenge. Cell viability was determined using a CCK-8 assay. Then, the levels of the oxidative stress-related factors were evaluated using corresponding kits. Pyroptosis was assessed by measurement of gasdermin-N domain (GSDMD-N) and caspase-1 (CASP1) expression. Subsequently, miR-16-5p expression was detected using RT-qPCR. The levels of oxidative stress and pyroptosis were examined after miR-16-5p silencing. The Starbase database predicted that CASP1 is a potential target of miR-16-5p, which was verified through a luciferase reporter assay. Moreover, CASP1 expression was determined after miR-16-5p silencing in HG-stimulated HRECs with puerarin exposure. Results revealed that puerarin significantly enhanced cell viability and inhibited oxidative stress. Furthermore, puerarin markedly downregulated GSDMD-N and CASP1 expression, and miR-16-5p level was notably inhibited in HG-stimulated HRECs, which was reversed after puerarin intervention. Following transfection with miR-16-5p inhibitor, the effects of puerarin on cell viability, oxidative stress and pyroptosis were attenuated in HG-induced HRECs. CASP1 was confirmed as a direct target gene of miR-16-5p. Taken together, puerarin alleviates oxidative stress and pyroptosis in HG-stimulated HRECs through regulating the miR-16-5p/CASP1 axis.

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Oxidative stress induced pyroptosis leads to osteogenic dysfunction of MG63 cells

Cited by 51 publications

References 46 publications

NLRP3 regulates alveolar bone loss in ligature‐induced periodontitis by promoting osteoclastic differentiation

NLRP3 regulates alveolar bone loss in ligature‐induced periodontitis by promoting osteoclastic differentiation

Inflammasomes in Alveolar Bone Loss

Puerarin protects against human retinal endothelial cells injury induced by high glucose via regulating miR-16-5p/CASP1 axis

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