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.
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 associated with periodontal bone tissue destruction in diabetic patients. SUMO modification has been reported in various diseases and are associated with an increasing number of biological processes, but previous studies have not focused on diabetic periodontitis.Methods: Periodontal membrane stem cells (PDLSCs) were isolated and cultured from healthy human obstructed teeth after extraction or adolescent orthodontic subtractive extraction. PDLSCs were cultured with medical 5% sterile glucose solution formulated as osteogenic differentiation induction solution with different glucose concentrations. The effects of different glucose concentrations on the osteogenic differentiation ability of PDLSCs were investigated at the genetic and cellular levels using staining assay, Western Blot, RT-PCR, Co-IP and cytofluorescence.Results: We found that SLUG, RUNX2 expression was decreased in PDLSCs cultured in high glucose osteogenic induction solution compared with normal glucose osteogenic induction solution. In addition, the IGF-1R expression levels, osteogenic differentiation and sumoylation of IGF-1R in PDLSCs cultured in high glucose osteogenic induction solution were not consistent with those cultured in normal glucose osteogenic induction solution.Conclusion: Our data demonstrated that SUMO1 modification of IGF-1R in high glucose environment inhibited osteogenic differentiation of PDLSCs by binding to SLUG, a key factor leading to periodontal bone tissue loss in diabetic patients. Thus we can maximize the control of multiple downstream damage signaling factors and bring new hope for periodontal tissue regeneration in diabetic patients.
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