Autophagy in periodontal disease: Evidence from a literature review

Lorenzo-Pouso, Alejandro I.; Castelo‐Baz, Pablo; Pérez‐Sayáns, Mario; Lim, Jason; Leira, Yago

doi:10.1016/j.archoralbio.2019.03.029

Cited by 13 publications

(7 citation statements)

References 145 publications

(148 reference statements)

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“…Until now, the significance of autophagy in periodontal diseases is not fully unraveled 11 . Autophagy may protect cells from apoptosis, increasing angiogenesis, while it may also trigger cell death, and facilitate immune evasion of bacteria 12 . Our present study indicated that NCOA4‐mediated ferritinophagy may increase free iron availability during inflammatory responses in host cells.…”

Section: Discussionmentioning

confidence: 59%

“…Autophagy is basically a cellular recycling pathway, and it also can defend host cells from invaded microbials by pathogen degradation 12 . Iron is critical to the survival of almost all living organisms; therefore, host cells may utilize iron that is stored in the ferritin when challenged by pathogens 27 .…”

Section: Discussionmentioning

confidence: 99%

“…The role of the selective microautophagy, including ferritinophagy, mitophagy (autophagy‐dependent elimination of mitochondria), and pexophagy (the selective removal of peroxisomes) in the progress of periodontal diseases was less clear 5 . Periodontitis progress is characterized by the activation of macroautophagy, and such autophagy may protect periodontal ligament stem cells from apoptosis in an inflammatory microenvironment 11,12 . Increased levels of autophagy gene expression were observed in peripheral blood mononuclear cells from patients with periodontitis compared with controls, 13 while lipopolysaccharide from P .…”

Section: Introductionmentioning

confidence: 99%

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NCOA4‐mediated ferritinophagy promoted inflammatory responses in periodontitis

Guo

Zhao

et al. 2021

J of Periodontal Research

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Background/Objectives Iron homeostasis plays a crucial role in the combat against pathogen invasion. Ferrous iron can trigger generous production of reactive oxygen species (ROS) by Fenton reaction. Nuclear receptor coactivator 4 (NCOA4), a selective cargo receptor to deliver ferritin to lysosome, may trigger release of ferritin‐bound iron into the cytosol. The aim of the present study was to explore whether NCOA4‐mediated ferritinophagy participated in the pathogenesis of periodontitis, and its role in promoting the periodontal inflammation. Methods Inflamed and healthy periodontal tissues were harvested for immunobiological staining of ferritinophagy‐related genes in the periodontal tissues, while real‐time quantitative PCR (qPCR) was utilized to detect mRNA transcription. Periodontal ligament fibroblasts (PDLFs) were isolated and infected with Porphyromonas gingivalis. The mRNA transcription and protein expression of genes involved in the iron metabolism, including NCOA4, transferrin receptor 1 (TFR1), and ferroportin (SLC40A1) were detected by qPCR and western blot. Levels of labile iron pool and ROS production were detected by flow cytometry and confocal endoscopy. Small interference RNA was utilized to knock down NCOA4. Results Elevated expression of NCOA4, ferritin heavy chain, and light chain were observed in the diseased periodontal tissues. P. gingivalis infection promoted expression of TFR1, NCOA4, and microtubule‐associated protein 1‐light chain 3 B (LC3B), enhanced levels of intracellular labile iron pool and ROS production. NCOA4 knockdown reduced ROS generation in PDLFs in response to P. gingivalis and mitigated production of pro‐inflammatory monocyte chemoattractant protein‐1 and interleukin 6. P. gingivalis triggered activation of c‐Jun N‐terminal kinase (JNK) and p38 mitogen‐activated protein kinase signaling pathway. In addition, inhibitors of JNK, SP600125, and inhibitors of p38, SB203580 blocked NCOA4 transcription. Conclusion NCOA4‐ferritinophagy participated in the progress of periodontitis progression. P. gingvalis‐triggered ferritinophagy aggravated production of ROS and inflammatory responses in PDLFS. These findings suggest iron homeostasis plays an important role in the pathogenesis of periodontitis.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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NCOA4‐mediated ferritinophagy promoted inflammatory responses in periodontitis

Guo

Zhao

et al. 2021

J of Periodontal Research

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“…Notably, disruption in the regulatory mechanisms of autophagy has been demonstrated in periodontitis ( Jiang et al, 2020 ). Meanwhile, numerous pharmaceutical and nutraceutical agents have been shown to modulate autophagy, thus serving as useful therapies for periodontitis ( Lorenzo-Pouso et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of oxytocin-related genes in periodontitis

Ghafouri‐Fard

Gholami

Nazer

et al. 2022

Front. Mol. Neurosci.

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Periodontitis is a common oral disorder leading to tooth loss in both developed and developing regions of the world. This multifactorial condition is related to the abnormal activity of several molecular pathways, among them are oxytocin-related pathways. In this study, we enrolled 26 patients and 28 controls and assessed the expression of four oxytocin-related genes, namely, FOS, ITPR, RCAN1, and RGS2, in circulation and affected tissues of enrolled individuals using real-time PCR. Expression of FOS was downregulated in total periodontitis tissues compared with total control tissues [ratio of mean expression (RME) = 0.23, P-value = 0.03]. Expression of FOS was also lower in total blood samples of patients compared with total controls. Expression of ITPR was downregulated in total periodontitis tissues compared with total control tissues (RME = 0.16, P-value = 0.01). Moreover, the expression of ITPR was reduced in total blood samples of patients compared with controls (RME = 0.25, P-value = 0.03). Expression of RCAN1 was downregulated in total periodontitis tissues compared with total control tissues (RME = 0.17, P-value = 0.01). However, the expression of RCAN1 was not different in blood samples of affected vs. unaffected individuals. Finally, the expression of RGS2 was lower in total periodontitis tissues compared with total control tissues (RME = 0.24, P-value = 0.01) and in total blood samples of affected individuals compared with controls (RME = 0.42, P-value = 0.05). This study provides data about the association between expressions of oxytocin-related genes and the presence of periodontitis. Future studies are needed to unravel the mechanistic links and find the correlation between expressions of these genes and the pathological stage of periodontitis.

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“…[5][6][7] Recent studies found that autophagy protects PDL stem cells from apoptosis and promotes angiogenesis in the inflammatory microenvironment. 6,8 Autophagy helps eliminate periodontal pathogen infection and modulates the immune inflammatory response in periodontitis. 9 However, the precise mechanism by which autophagy is regulated under inflammatory conditions remains unclear.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Non-Coding RNA H19 Participates in Periodontal Inflammation via Activation of Autophagy</p>

Guo

Huang

Líu

et al. 2020

JIR

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Purpose: Periodontitis is the leading cause of tooth loss. The role of long non-coding RNA (lncRNA) in periodontal inflammation remains unclear. The aim of this study was to investigate the role of lncRNA H19 in periodontitis and its possible regulation of autophagy in periodontitis. Material and Methods: Inflammation level was determined by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) in periodontal ligament cells (PDLCs). Western blotting, flow cytometric analysis, and immunofluorescence staining were used to detect the autophagy flux. Overexpression or knockdown of H19 was used to confirm its function. Ligature-induced periodontitis model in mice and periodontitis-affected human gingival tissue were used in vivo. RNA sequencing was performed to determine the differentially expressed genes. Results: Autophagy was significantly increased in PDLCs after inflammatory stimulation as well as in a ligature-induced periodontitis model in mice and periodontitis-affected human gingival tissue. During the inflammatory process, H19 expression was also significantly upregulated. Further, the levels of autophagic markers were significantly upregulated after overexpressing H19 in PDLCs, and the increased autophagic activity induced by inflammatory stimulation was reversed by H19 knockdown. RNA sequencing showed that the expression profiles of mRNAs were significantly altered after H19 overexpression, and the differentially expressed genes were enriched in the PI3K/AKT signaling pathway, which was confirmed by the decreased p-AKT protein expression in the H19 overexpression group. Conclusion: Periodontal inflammation activates autophagy flux, and H19 mediates the activation of autophagy via AKT pathway in periodontitis. This study expands our understanding of molecular regulation in periodontitis.

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Autophagy in periodontal disease: Evidence from a literature review

Cited by 13 publications

References 145 publications

NCOA4‐mediated ferritinophagy promoted inflammatory responses in periodontitis

NCOA4‐mediated ferritinophagy promoted inflammatory responses in periodontitis

Downregulation of oxytocin-related genes in periodontitis

<p>Long Non-Coding RNA H19 Participates in Periodontal Inflammation via Activation of Autophagy</p>

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