Autophagy and its significance in periodontal disease

Yang, Yuhui; Huang, Yiping; Li, Wei-ran

doi:10.1111/jre.12810

Cited by 31 publications

(31 citation statements)

References 116 publications

(252 reference statements)

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“…Autophagy plays an important role in the occurrence and development of in ammation and immune response [33]. In recent years, more and more studies in vitro and in vivo have con rmed the role of autophagy in periodontitis [9], but there is no su cient evidence to con rm whether the role of autophagy in periodontitis is protective or pathological [34,35]. An et al [36] reported that autophagy disorder in periodontitis was associated with protection.…”

Section: Discussionmentioning

confidence: 99%

Nicotine Regulates Autophagy of Human Periodontal Ligament Cells Through α7 nAchR That Promotes Secretion of Inflammatory Factors IL-1β and IL-8

Yang

Zhou³

et al. 2021

Preprint

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Backgroud: Nicotine is an important risk factor and the main toxic component associated with periodontitis. However, the mechanism of nicotine induced periodontitis is not clear. To investigated the mechanism through which nicotine regulates autophagy of human periodontal ligament cells (hPDLCs) through the alpha7 nicotinic acetylcholine receptor (α7 nAChR) and how autophagy further regulates the release of IL-1β and IL-8 secretion in hPDLCs. Methods: HPDLCs were obtained from root of extracted teeth and pre-incubated in alpha-bungarotoxin (α-BTX) or 3-Methyladenine (3-MA), followed by culturing in nicotine. We used a variety of experimental detection techniques including western blotting, immunofluorescence, enzyme-linked immunosorbent assay (ELISA), transmission electron microscopy (TEM) and RT-qPCR to assess the expression of the LC3 protein, autolysosome, and release of IL-1β and IL-8 from hPDLCs. Results: Western blots, immunofluorescence and TEM results found that the nicotine significantly increased the autophagy expression in hPDLCs that was time and concentration dependent and reversed by α-BTX treatment (p﹤0.05). RT-qPCR and ELISA results revealed a noticeable rise in the release of inflammatory factors IL–1β and IL-8 from hPDLCs in response to nicotine. RT-qPCR and ELISA results showed that nicotine can significantly up-regulate the release of inflammatory factors IL-1β and IL-8 in hPDLCs, and this effect can be inhibited by 3-MA (p﹤0.05).Conclusions: Nicotine regulated autophagy of hPDLCs through α7 nAChR and in turn the regulation of the release of inflammatory factors 1L-1β and 1L-8 by hPDLCs.

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Section: Discussionmentioning

confidence: 99%

Nicotine Regulates Autophagy of Human Periodontal Ligament Cells Through α7 nAchR That Promotes Secretion of Inflammatory Factors IL-1β and IL-8

Yang

Zhou³

et al. 2021

Preprint

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“…UNC-51-like kinase (ULK)/ ATG1 is a key protein that initiates autophagy by forming a complex with ATG13, ATG101, and focal adhesion kinase family interacting protein of 200 kD (FIP200) to induce autophagic signals. 3 The class-III phosphatidylinositol 3-kinase (PI3K) complex composed of Beclin1/ATG6, vesicular protein sorting (Vps) 34, Vps15, and ATG14, induces the production of phosphatidylinositol-3-phosphate to recruit effectors required for the formation of autophagosomes. ATG9 is a transmembrane protein and its bidirectional movement between phagophore assembly sites (PASs) and non-PASs contributes to the delivery of membranous structures to form autophagosomes.…”

Section: Figure 1: Three Types Of Autophagymentioning

confidence: 99%

“…The induced autophagy in GECs provides a favourable microenvironment for its persistence and evasion of immune defense. 3…”

Section: Figure 6: Schematic Representation Of the Junctional Epithelium Keratinocytes-autophagy Induced By A Actinomycetemcomitans Infecmentioning

confidence: 99%

“…PI3K/ protein kinase B (Akt)/mTOR signalling pathway is a critical regulator of autophagy and inactivation of it results in autophagy after P.g invading. 3 Moreover, Pg in the cytosol is usually degraded by lysosomes, but the ratio of free Pg in the cytosol is low compared with Pg co-localized with double-membrane vacuoles. Thereby, most co-localized Pg evades host defenses by impairs the formation of autolysosomes which leads to accumulating autophagosomes that supply nutrients for bacteria survival.…”

Section: Porphyromonas Gingivalis (Pg)mentioning

confidence: 99%

“…The integration of autophagy into these biological functions and other stress responses is determined by the transcriptional factors that undertake the regulatory mechanism. 3 Autophagy, as a strictly regulated catabolic process mediating cellular degradation and recycling, is crucial for maintaining homeostasis and development. The autophagic process is thought to be a form of endogenous defense mechanism that allows cells to survive during harsh conditions, including hypoxia, heat, starvation, and oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

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Dual Role of Autophagy in Periodontal Disease

Muwal¹,

Kaur²,

Kaur³

2021

ijmsdr

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Autophagy is a self-degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress. The induction of autophagy has been shown to have both protective and pathological effects in periodontitis. Autophagy also plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles, such as mitochondria, endoplasmic reticulum and peroxisomes, as well as eliminating intracellular pathogens. Thus, autophagy is generally thought of as a survival mechanism, although its deregulation has been linked to non-apoptotic cell death. Autophagy is an evolutionarily conserved process essential for cellular homeostasis and human health. Autophagy provides a mechanism for the turnover of cellular organelles and proteins through a lysosome-dependent degradation pathway. It also participates in various biological processes, such as cellular differentiation, cell function, and defense against pathogens. In addition, autophagic dysfunction is associated with multiple diseases such as autoimmune disease, cancer, diabetes, and oral disease. Nowadays research has ascertained the role of autophagy in Periodontal disease, especially its role in the host defence against periodontal disease drivers. A bulk of research has recognized several pharmaceuticals and nutraceuticals that can potentially modulate this kind of cell death and serve as useful therapies. However, further research is warranted in order to reach a clinical translation, which could be of help in the discovery of novel host modulation therapies for Periodontal disease. Keywords: Autophagy, Apoptosis, Micro autophagy, immune response, Periodontitis, Periodontal pathogens, Periapical lesion

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Argpyrimidine bonded to RAGE regulates autophagy and cell cycle to cause periodontal destruction

Dong

Gao

et al. 2022

Journal Cellular Physiology

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Argpyrimidine (APMD), a methylglyoxal-arginine-derived product, is one of the main products of diabetes mellitus. We aimed to systematically investigate the role of APMD in regulating autophagy activity, with a specific focus on the finding of APDM binding molecule, matching amino acid residues, autophagy flux and proteins, cell cycle arrest, cell skeleton and migration, PI3K/AKT/mTOR pathways, inflammatory signals, alveolar bone destruction, and inhibition verification. In this study, binding to 59/94/121 amino acid residues of advanced glycosylation end product receptor (RAGE), APMD suppressed PI3K/AKT/mTOR pathway to attenuate cell survival of periodontal ligament cells (PDLCs). Simultaneously, autophagy proteins ATG5, Beclin1, and LC3-II/I expression ratio were upregulated while P62/SQSTM was downregulated. Cell cycle arrested at G0/G1 with enhancing Cyclin D1/CDK4 and decreasing Cyclin A/CDK2 expression. Inhibition of autophagy abrogated APMDinduced cell cycle arrest. Furthermore, the inflammation regulation network of matrix metalloproteinase (MMP)-2, MMP-9, MAPKs and NF-κB pathways were activated by APMD. Rat periodontal models confirmed that APMD induced alveolar bone resorption, increased inflammatory infiltrates, and degraded collagen fibers through RAGE and PI3K. APMD-induced autophagy, G0/G1 arrest, proinflammatory signals activating and periodontal destruction were reversed by RAGE knockdown while aggravated by PI3K inhibitor. This study provides the first evidence that APMD bind to RAGE to regulate autophagy and cell cycle of PDLCs through the PI3K/AKT/mTOR pathway, thereby promoting periodontal destruction.

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Autophagy and its significance in periodontal disease

Cited by 31 publications

References 116 publications

Nicotine Regulates Autophagy of Human Periodontal Ligament Cells Through α7 nAchR That Promotes Secretion of Inflammatory Factors IL-1β and IL-8

Nicotine Regulates Autophagy of Human Periodontal Ligament Cells Through α7 nAchR That Promotes Secretion of Inflammatory Factors IL-1β and IL-8

Dual Role of Autophagy in Periodontal Disease

Argpyrimidine bonded to RAGE regulates autophagy and cell cycle to cause periodontal destruction

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