Overexpression of Cyclophilin A in Human Periapical Lesions

Wang, Yanqing; Liu, Guojing; Zhang, Jie; Zhu, Lingxin; Yu, Jingjing; Zhu, Shenting; Lv, Fengyuan; Peng, Bin

doi:10.1016/j.joen.2019.09.006

Cited by 7 publications

(9 citation statements)

References 35 publications

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“…It has been reported that apolipoprotein E controls cerebrovascular integrity via CypA in Alzheimer's disease (Bell et al, 2012;Montagne et al, 2020). Moreover, it is well established that CypA is a pro-inflammatory agent and has been considered as a marker of RA (Dongsheng et al, 2017), sepsis (Jiang et al, 2018), asthma (Chen et al, 2021), and periodontitis (Wang et al, 2019;Xue et al, 2018). The progress of acute inflammation includes three phases: activation, resolution, and remodeling homeostasis.…”

Section: Discussionmentioning

confidence: 99%

Delicate regulation of IL-1β-mediated inflammation by cyclophilin A

et al. 2022

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Section: Discussionmentioning

confidence: 99%

Delicate regulation of IL-1β-mediated inflammation by cyclophilin A

et al. 2022

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“…Immunofluorescence double staining was performed as previously described (Wang et al, 2019a, 2019b, 2019c). In a typical procedure, after deparaffinization and rehydration, sections were incubated with pepsin (Maixin) for 30 min.…”

Section: Methodsmentioning

confidence: 99%

“…Immuno‐positive cells were quantified using Image‐Pro Plus version 6.0 (Media Cybernetics, Inc.) with images of stained slides captured by fluorescent microscopy (Leica). Each sample was randomly divided into three fields, each field was photographed at 400× magnification (0.0714 mm 2 /field) under different wavelengths with the slide remaining stationary (Wang et al, 2019a, 2019b, 2019c). Images were superimposed and screened using the Photoshop software (Adobe Systems Incorporated) to disclose positive cells.…”

Section: Methodsmentioning

confidence: 99%

“…The mechanisms through which mitochondria‐derived modulations affect the protective immune response of macrophages remain unclear. However, increasing evidence indicates that PTEN‐induced putative kinase 1 (PINK1) and Parkin E3 ubiquitin‐protein ligase (Parkin) are closely involved (Hung et al, 2021; Wang et al, 2019a, 2019b, 2019c). PINK1 and Parkin are expressed in many types of cell.…”

Section: Introductionmentioning

confidence: 99%

“…The expression levels of PINK1 and Parkin were reported to increase in macrophages after LPS stimulation, and the observed increase in PINK1 and Parkin expression could promote the recovery of acute lung injury induced by sepsis (Chen et al, 2021; Shi et al, 2019). PINK1 knockdown with PINK1 siRNA leads to aggravated inflammation in macrophages after LPS stimulation (Wang et al, 2019a, 2019b, 2019c). Coincidentally, macrophages derived from Park2 −/− and Pink1 −/− mice display increased release of IL‐1β and IL‐18, which has also been observed in the macrophages from patients with PARK2 mutations (Mouton‐Liger 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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