Background Periodontal disease, an oral disease characterized by loss of alveolar bone and progressive teeth loss, is the sixth major complication of diabetes. It is spreading worldwide as it is difficult to be cured. The insulin-like growth factor 1 receptor (IGF-1R) plays an important role in regulating functional impairment associated with diabetes. However, it is unclear whether IGF-1R expression in periodontal tissue is related to alveolar bone destruction in diabetic patients. SUMO modification has been reported in various diseases and is associated with an increasing number of biological processes, but previous studies have not focused on diabetic periodontitis. This study aimed to explore the role of IGF-1R in osteogenic differentiation of periodontal ligament stem cells (PDLSCs) in high glucose and control the multiple downstream damage signal factors. Methods PDLSCs were isolated and cultured after extraction of impacted teeth from healthy donors or subtractive orthodontic extraction in adolescents. PDLSCs were cultured in the osteogenic medium with different glucose concentrations prepared by medical 5% sterile glucose solution. The effects of different glucose concentrations on the osteogenic differentiation ability of PDLSCs were studied at the genetic and cellular levels by staining assay, Western Blot, RT-PCR, Co-IP and cytofluorescence. Results We found that SNAI2, RUNX2 expression decreased in PDLSCs cultured in high glucose osteogenic medium compared with that in normal glucose osteogenic medium, which were osteogenesis-related marker. In addition, the IGF-1R expression, sumoylation of IGF-1R and osteogenic differentiation in PDLSCs cultured in high glucose osteogenic medium were not consistent with those cultured in normal glucose osteogenic medium. However, osteogenic differentiation of PDLCSs enhanced after adding IGF-1R inhibitors to high glucose osteogenic medium. Conclusion Our data demonstrated that SUMO1 modification of IGF-1R inhibited osteogenic differentiation of PDLSCs by binding to SNAI2 in high glucose environment, a key factor leading to alveolar bone loss in diabetic patients. Thus we could maximize the control of multiple downstream damage signaling factors and bring new hope for alveolar bone regeneration in diabetic patients.
In the oral microenvironment, bacteria colonies are easily aggregated on the tooth-restoration surface, in the manner of a biofilm, which usually consists of heterogeneous structures containing clusters of a variety of bacteria embedded in an extracellular matrix, leading to serious recurrent caries. In this contribution, zero-dimensional (0D) bismuth (Bi) quantum dots (QDs) synthesized by a facile solvothermal method were directly employed to fabricate a Bi QD/polydimethylsiloxane (PDMS)-modified tooth by simple curing treatment. The result demonstrates that the as-fabricated Bi QD/PDMS-modified tooth at 37 °C for 120 min not only showed significantly improved hydrophobic performance with a water contact angle of 103° and 115° on the tooth root and tooth crown, respectively, compared to that (~20° on the tooth root, and ~5° on the tooth crown) of the pristine tooth, but also exhibited excellent antibacterial activity against S. mutans, superior biocompatibility, and biosafety. In addition, due to the highly photothermal effect of Bi QDs, the antibacterial activity of the as-fabricated Bi QD/PDMS-modified tooth could be further enhanced under illumination, even at a very low power density (12 mW cm−2). Due to the facile fabrication, excellent hydrophobicity, superior antibacterial activity, and biocompatibility and biosafety of the Bi QD/PDMS-modified tooth, it is envisioned that the Bi QD/PDMS-modified tooth with a fascinating self-cleaning and antibacterial performance can pave the way to new designs of versatile multifunctional nanocomposites to prevent secondary caries in the application of dental restoration.
The bacterial accumulation at the margins of dental resin composites is a main cause of secondary caries, which may further lead to prosthodontic failure. In this regard, this study for the first time incorporated 2D MXene Ti3C2Tx nanosheets (NSs) into epoxy resin at different mass ratios (0, 0.5, 1.0, and 2.0 wt%) by solution blending and direct curing for dental applications. Compared to the pure resin, the as-fabricated MXene/resin composite not only exhibited improved mechanical and abrasive results but also displayed gradually improved antibacterial activity with MXene loading which was further enhanced by illumination in natural light due to the high photothermal efficiency of MXene. In addition, the cytotoxicity result demonstrated that the MXene-modified resin did not cause severe damage to normal cells. This novel MXene/resin nanocomposite could pave the way for new designs for high-performance, multifunctional nanocomposites to effectively protect dental health in daily life.
TEAD4 is a member of the TEA domain (TEAD) family of transcription factors. It plays a key regulatory role in embryonic development, tissue homeostasis and cancer progression. Its expression is related to the regulation of a variety of inflammations. MicroRNA can regulate the expression of target genes and play an important role in various physiological and pathological processes. In view of the important role of TEAD4 and microRNA-629-5p (miR-629-5p) in inflammation, and based on the findings of bioinformatics research, we selected miR-629-5p as the focus of our study. In inflammatory dental pulp, we found that the expression of miR-629-5p was increased, while the expression of TEAD4 was decreased. We used Porphyromonas gingivalis lipopolysaccharide (LPS) as a stimulator of dental pulp stem cells (DPSCs) to simulate the inflammatory environment of dental pulp. The mineralization ability of LPS-stimulated DPSCs was significantly inhibited, while the level of miR-629-5p increased and the level of TEAD4 decreased. Inhibition of miR-629-5p can reverse the odontogenic defects of DPSCs treated with LPS. In addition, the expression of miR-629-5p in DPSCs was negatively correlated with the expression of TEAD4. In conclusion, miR-629-5p can inhibit the odontogenic differentiation of human dental pulp stem cells and the mechanism may be related to its role in downregulation of TEAD4 expression.
Background: Impairment of lineage specification and function of gonadal somatic cells can lead to disorders of sexual development (DSDs) and fertility defects in humans. However, little is known about the function of protein phosphatases in testis development. Results: We showed that protein phosphatase 4 (PPP4) could maintain SOX9 expression in Sertoli cells and play an essential role in Sertoli cell lineage maintenance and male fertility. Conditional deletion of Ppp4c, a PPP4 catalytic subunit gene, caused the reprogramming of Sertoli cells to granulosa-like cells postnatally by inducing ectopic expression of FOXL2, which in turn led to testicular BTB structure damage, germ cell loss and ultimate testis to ovary-like gland transformation. Conclusion: Reprogramming of Sertoli cells due to absence of PPP4 may help explain the etiology of disorders of sexual differentiation and male infertility.
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