The Expression of Interferon Regulatory Factor 8 in Human Periapical Lesions

Yu, Jingjing; Liu, Mingwen; Zhu, Lingxin; Zhu, Shenting; Lv, Fengyuan; Wang, Yanqing; Wang, Li; Peng, Bin

doi:10.1016/j.joen.2018.04.015

Cited by 8 publications

(14 citation statements)

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“…The macrophage is one of the most plastic cells in periapical lesions (Yu et al, 2018), and CD68 is considered as a marker of inflammation associated with macrophages (Chistiakov et al, 2017). Accordingly, whether the expression of PINK1, Parkin and LC3 was affected in macrophages of human apical periodontitis lesions was investigated through double staining PINK1, Parkin and LC3 with CD68.…”

Section: Resultsmentioning

confidence: 99%

“…The quantitative analysis was performed as previously described (Yu et al, 2018). Briefly, five views of every section were randomly selected under 400× magnification following the same standards using light microscopy (Olympus).…”

Section: Immunohistochemical Stainingmentioning

confidence: 99%

“…Apical periodontitis, primarily attributed to complex microbial infections, has been shown to be a host response to the invasion of microbes in the root canal (Huang et al, 2018; Yu et al, 2018). Periapical granulomas (PGs) and radicular cysts (RCs) are the two representative pathological forms of periapical lesions (Huang et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…They are recruited to the infected areas and activated by interferon‐gamma (IFN‐γ) and bacterial lipopolysaccharide (LPS). They then secrete high levels of proinflammatory cytokines, such as tumour necrosis factor‐α (TNF‐α), IL‐1β and IL‐6 during the initial phase of periapical inflammation (Shapouri‐Moghaddam et al, 2018; Yu et al, 2018). Meanwhile, macrophages produce reactive oxygen species (ROS) and mediate ROS‐induced tissue damage during infection (Shapouri‐Moghaddam et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

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Expression of PINK1 and Parkin in human apical periodontitis

et al. 2022

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Aim: PTEN-induced putative kinase 1 (PINK1) and Parkin E3 ubiquitin-protein ligase (Parkin) are critical for immune and inflammatory regulation in health and disease. PINK1 and Parkin have been confirmed to be involved in the progression of apical periodontitis by affecting mitophagy-related osteoblast apoptosis; however, the expression of PINK1 and Parkin in macrophages, one of the most important cells in apical periodontitis, remains unknown. This study aimed to investigate the expression of PINK1 and Parkin in human apical periodontitis lesions, as well as their possible localization in macrophages. Methodology: Thirty-seven human periapical tissues, including periapical granulomas (PGs, n = 12), radicular cysts (RCs, n = 11) and healthy gingival tissues (n = 14) were examined. The inflammatory infiltrates of lesions were evaluated by haematoxylin staining, and the expression of PINK1 and Parkin was detected by immunohistochemistry. Double immunofluorescence was used to explore the colocalization of microtubule-associated protein 1 light chain 3 (LC3) and TOMM20, as well as the localization of PINK1 and Parkin, in macrophages of human apical periodontitis lesions. The ultrastructural morphology of mitochondria in human apical periodontitis lesions was visualized by transmission electron microscopy (TEM). Data were analysed by one-way anova with Student-Newman-Keul's test and the Mann-Whitney test. p < .05 was considered statistically significant. Results: Immunohistochemistry demonstrated a significantly higher expression of PINK1 and Parkin proteins in human apical periodontitis lesions than in healthy gingival tissues (p < .0001), but no significant difference was demonstrated between PGs and RCs (p > .05). The higher expression of LC3 and the presence of more LC3-TOMM20 double-positive cells were also observed in human apical periodontitis. Double-labelling analysis of PINK1, Parkin and LC3 with CD68 indicated that macrophage mitophagy might be present in the progression of human apical periodontitis. Finally, the results of TEM morphological analysis revealed the appearance of double-membraned mitophagosomes and vacuolated mitochondria in macrophagelike cells of apical periodontitis lesions. Conclusions: Our findings indicated that PINK1 and Parkin proteins were highly expressed in clinical apical periodontitis lesions.

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Section: Resultsmentioning

confidence: 99%

Section: Immunohistochemical Stainingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Expression of PINK1 and Parkin in human apical periodontitis

et al. 2022

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“…The tooth sections were double-labeled with BACH1 and HO-1 as the previous approach [20]. Briefly, after deparaffinization and rehydration, the sections were treated with EDTA antigen retrieval solution was used at 95 ℃ for 30 min.…”

Section: Double Immunofluorescence Labellingmentioning

confidence: 99%

BACH1 regulates the proliferation and odontoblastic differentiation of human dental pulp stem cells

Liu

et al. 2022

BMC Oral Health

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Background The preservation of biological and physiological vitality as well as the formation of dentin are among the main tasks of human dental pulp for a life time. Odontoblastic differentiation of human dental pulp stem cells (hDPSCs) exhibits the capacity of dental pulp regeneration and dentin complex rebuilding. Exploration of the mechanisms regulating differentiation and proliferation of hDPSCs may help to investigate potential clinical applications. BTB and CNC homology 1 (BACH1) is a transcription repressor engaged in the regulation of multiple cellular functions. This study aimed to investigate the effects of BACH1 on the proliferation and odontoblastic differentiation of hDPSCs in vitro. Methods hDPSCs and pulpal tissues were obtained from extracted human premolars or third molars. The distribution of BACH1 was detected by immunohistochemistry. The mRNA and protein expression of BACH1 were examined by qRT-PCR and Western blot analysis. BACH1 expression was regulated by stable lentivirus-mediated transfection. Cell proliferation and cell cycle were assessed by cell counting kit-8 assay, 5-Ethynyl-2'-deoxyuridine assay and flow cytometry. The expression of mineralization markers, alkaline phosphatase (ALP) activity and alizarin red S staining were conducted to assess the odontoblastic differentiation ability. Results BACH1 expression was stronger in the odontoblast layer than in the cell rich zone. The total and nuclear protein level of BACH1 during odontoblastic differentiation was downregulated initially and then upregulated gradually. Knockdown of BACH1 greatly inhibited cell proliferation, arrested cell cycle, upregulated the heme oxygenase-1 (HO-1) expression and attenuated ALP activity, decreased calcium deposits and downregulated the expression of mineralization markers. Treatment of Tin-protoporphyrin IX, an HO-1 inhibitor, failed to rescue the impaired odonto/osteogenic differentiation capacity. Overexpression of BACH1 increased cell proliferation, ALP activity and the expression of mineralization markers. Conclusions Our findings suggest that BACH1 is an important regulator of the proliferation and odontoblastic differentiation of hDPSCs in vitro. Manipulation of BACH1 expression may provide an opportunity to promote the regenerative capacity of hDPSCs.

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