International endodontic journal · 2014
Kinetics of glycogen synthase kinase (GSK)3β and phosphorylated GSK3β (Ser 9) expression in experimentally induced periapical lesions.
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Sun Z, Wang L, Peng B
Аннотация
AIM: To investigate the kinetics of GSK3β and p-GSK3β (Ser 9) expression in experimentally induced rat periapical lesions and to explore their possible functions in the pathogenesis of periapical lesions.
METHODOLOGY: Periapical lesions were established in Wistar rats by occlusal pulp exposure in mandibular first molar teeth. The animals were killed on days 0, 7, 14, 21 and 28. Micro-computed tomographic, histological and enzyme histochemical analyses were performed to detect the progression of periapical lesions. Immunohistochemistry, double-dye immunofluorescence and Western blot were performed to determine the expression of GSK3β and p-GSK3β (Ser 9) in periapical tissues.
RESULTS: From day 0 to day 28, the lesion volume and area gradually expanded, and the GSK3β-positive cells gradually ascended. A few p-GSK3β (Ser 9)-positive cells and osteoclasts appeared on day 7 and then climaxed on day 14. The numbers then simultaneously decreased from day 21 to day 28. Western blot analysis revealed that p-GSK3β (Ser 9) and GSK3β proteins were expressed at all time-points. The positive cells and protein expression ratio of p-GSK3β (Ser 9) against GSK3β increased from day 0 to day 14 and then decreased from day 14 to day 28. Finally, double-dye immunofluorescence assay revealed that p-GSK3β (Ser 9)-positive and RANKL-positive cells were co-localized around periapical lesions on days 14 and 28.
CONCLUSIONS: GSK3β and p-GSK3β (Ser 9) can be observed and may be involved in alveolar bone resorption and inflammatory response in periapical lesions, as well as associated with periapical lesion pathogenesis.
METHODOLOGY: Periapical lesions were established in Wistar rats by occlusal pulp exposure in mandibular first molar teeth. The animals were killed on days 0, 7, 14, 21 and 28. Micro-computed tomographic, histological and enzyme histochemical analyses were performed to detect the progression of periapical lesions. Immunohistochemistry, double-dye immunofluorescence and Western blot were performed to determine the expression of GSK3β and p-GSK3β (Ser 9) in periapical tissues.
RESULTS: From day 0 to day 28, the lesion volume and area gradually expanded, and the GSK3β-positive cells gradually ascended. A few p-GSK3β (Ser 9)-positive cells and osteoclasts appeared on day 7 and then climaxed on day 14. The numbers then simultaneously decreased from day 21 to day 28. Western blot analysis revealed that p-GSK3β (Ser 9) and GSK3β proteins were expressed at all time-points. The positive cells and protein expression ratio of p-GSK3β (Ser 9) against GSK3β increased from day 0 to day 14 and then decreased from day 14 to day 28. Finally, double-dye immunofluorescence assay revealed that p-GSK3β (Ser 9)-positive and RANKL-positive cells were co-localized around periapical lesions on days 14 and 28.
CONCLUSIONS: GSK3β and p-GSK3β (Ser 9) can be observed and may be involved in alveolar bone resorption and inflammatory response in periapical lesions, as well as associated with periapical lesion pathogenesis.