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Aim: To investigate the specific role of arrestin beta‐2 (ARRB2) in the progression of periodontitis and the underlying mechanisms. Materials and Methods: Single‐cell RNA sequencing data were used to analyse gene expression in periodontal tissues from healthy controls and patients with periodontitis. Real‐time quantitative polymerase chain reaction, Western blotting and immunohistochemical staining were performed to detect the expression of ARRB2. Furthermore, a ligature‐induced periodontitis model was created. Using radiographic and histological methods, RNA sequencing and luciferase assay, the role of ARRB2 in periodontitis and the underlying mechanisms were explored. Finally, the therapeutic effect of melatonin, an inhibitor of activating transcription factor 6 (ATF6), on periodontitis in mice was assessed in both in vivo and in vitro experiments. Results: ARRB2 expression was up‐regulated in inflammatory periodontal tissue. In the ligature‐induced mouse model, Arrb2 knockout exacerbated alveolar bone loss (ABL) and extracellular matrix (ECM) degradation. ARRB2 exerted a negative regulatory effect on ATF6, an essential targeted gene. Melatonin ameliorated ABL and an imbalance in ECM remodelling in Arrb2‐deficient periodontitis mice. Conclusions: ARRB2 mediates ECM remodelling via inhibition of the ATF6 signalling pathway, which ultimately exerts a protective effect on periodontal tissues. [ABSTRACT FROM AUTHOR]

Objectives: Epulis is considered to be a massive reactive lesion rather than a true neoplasia. AhR is thought to be associated with inflammation and development of neoplasms. Here, we aimed to observe the expression of AhR in fibrous epulis and explore its role and possible mechanism in the pathogenesis of epulis. Materials and Methods: Epulis and normal gingival tissues were collected, and AhR expression was detected at the mRNA and protein levels by quantitative polymerase chain reaction (qPCR) and immunohistochemistry, respectively. The expression levels of proinflammatory cytokines and apoptosis‐related factor genes in human periodontal ligament cells (hPDLCs) and human gingival fibroblasts (hGFs) transfected with AhR short interfering RNA (siRNA) or negative control siRNA, upon stimulation with lipopolysaccharide of Porphyromonas gingivalis (Pg‐LPS), were then examined. Finally, the expression levels of the proinflammatory cytokines and apoptosis‐related factor genes in the epulis tissues were observed by qPCR. Results: AhR expression in fibrous epulis was significantly increased at both the mRNA and protein levels. The expression of proinflammatory cytokines and apoptosis‐related factor genes in hPDLCs transfected with AhR siRNA was significantly decreased when stimulated with Pg‐LPS. The same trends were observed for hGFs. The opposite trend was detected in the epulis tissues. Conclusion: AhR may be a key factor in fibrous epulis pathogenesis that acts by regulating the expression of BCL2 family genes and inflammatory factor‐related genes. [ABSTRACT FROM AUTHOR]

Objective: The involvement of lysosomal integral membrane protein 2 (LIMP2) in cholesterol transport and formation of foam cells under the infection of Porphyromonas gingivalis (P. gingivalis) is yet to be elucidated. The current study verified the role and explored the mechanism of LIMP2 in promoting foam cell formation by P. gingivalis. Background: An association between periodontitis and atherosclerosis (AS) has been established. P. gingivalis is a key pathogen of periodontitis that promotes foam cell formation by regulating activities of CD36 scavenger receptors expressed on the macrophages. LIMP2, a member of CD36 superfamily, is involved in cholesterol efflux. However, whether LIMP2 is involved in the formation of foam cells promoted by P. gingivalis remains unclear. Methods: The formation of foam cells was examined by Oil Red O staining. The knockdown of limp2 was identified by qRT‐PCR. The accumulation of cholesterol was monitored by Cholesterol Assay Kit. The location of P. gingivalis was visualized by confocal microscopy. Cathepsin L activity was monitored with Magic Red Cathepsin L Assay Kit. The key genes and pathways in P. gingivalis‐infected macrophages were explored by RNA sequencing. The protein level was investigated by Western blotting. Results: Porphyromonas gingivalis increases foam cells formation and upregulates the expression of LIMP2 in foam cells. The knockdown of limp2 decreases the number of foam cells and increases cholesterol export, which is related to lysosomal functions. In addition, the interaction between LIMP2 and caveolin‐1(CAV1) might contribute to this process, and NF‐κB and JNK activity is required for increased expression of P. gingivalis‐induced LIMP2. Conclusions: This study suggested that LIMP2 is involved in the foam cells formation facilitated by P. gingivalis, which favors a close connection between periodontitis and atherosclerosis (AS). [ABSTRACT FROM AUTHOR]

Oil-water separation has recently become a worldwide challenge due to the frequent occurrence of oil spill accidents and increasing industrial oily wastewater. In this work, the multifunctional mesh films with underwater oleophobicity and certain bacteriostatic effects are prepared by layer-by-layer assembly of graphene oxide-silica coatings on stainless steel mesh. The mesh film exhibits excellent environmental stability under a series of harsh conditions. The new, facile and reusable separation system is proposed to achieve deep treatment of oily wastewater, and the oil collection rate can reach over 99%.