Journal of oral biosciences · 2026
Gb3 synthase accelerates bone wound healing by promoting the proliferation and migration of osteoblasts.
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Sana Airi, Nagao Mayu, Furukawa Koichi, Sato Takuma, Tabuchi Masako, Miyazawa Ken, Hamamura Kazunori
Аннотация
OBJECTIVES: Bone formation in murine femoral cancellous bone is attenuated in Gb3 synthase knockout (Gb3S KO) mice deficient in Gb4 (globoside), a globo-series glycosphingolipid. However, whether Gb3S promotes bone wound healing is unclear. Therefore, we investigated the role of Gb3S in bone wound healing.
METHODS: The expression of Gb4 was analyzed using flow cytometry. The number of calvarial osteoblasts was measured in 8-week-old wild-type (WT) and Gb3S KO mice using hematoxylin and eosin-stained slides. A calvarial bone defect, namely, a 5-mm hole in the parietal region of the calvaria, was created in 8-week-old WT and Gb3S KO mice using a trephine bur. Micro computed tomography was performed at 0 and 12 weeks post-operatively to assess the bone wound healing. Cell proliferation and migration were analyzed using bromodeoxyuridine and wound healing motility assays, respectively. To investigate the regulation of Gb4-induced osteoblast proliferation, calvarial osteoblasts from Gb3S KO mice were treated with Gb4.
RESULTS: The number of calvarial osteoblasts from Gb3S KO mice was significantly lower than that from WT mice. Furthermore, bone wound healing was significantly delayed in Gb3S KO mice. The proliferation and migration of calvarial osteoblasts from Gb3S KO mice were significantly lower than those from WT mice. Moreover, the proliferation of calvarial osteoblasts from Gb3S KO mice was promoted by Gb4 treatment.
CONCLUSIONS: The results revealed that the expression of Gb3S promoted the proliferation and migration of osteoblasts, which accelerated bone wound healing.
METHODS: The expression of Gb4 was analyzed using flow cytometry. The number of calvarial osteoblasts was measured in 8-week-old wild-type (WT) and Gb3S KO mice using hematoxylin and eosin-stained slides. A calvarial bone defect, namely, a 5-mm hole in the parietal region of the calvaria, was created in 8-week-old WT and Gb3S KO mice using a trephine bur. Micro computed tomography was performed at 0 and 12 weeks post-operatively to assess the bone wound healing. Cell proliferation and migration were analyzed using bromodeoxyuridine and wound healing motility assays, respectively. To investigate the regulation of Gb4-induced osteoblast proliferation, calvarial osteoblasts from Gb3S KO mice were treated with Gb4.
RESULTS: The number of calvarial osteoblasts from Gb3S KO mice was significantly lower than that from WT mice. Furthermore, bone wound healing was significantly delayed in Gb3S KO mice. The proliferation and migration of calvarial osteoblasts from Gb3S KO mice were significantly lower than those from WT mice. Moreover, the proliferation of calvarial osteoblasts from Gb3S KO mice was promoted by Gb4 treatment.
CONCLUSIONS: The results revealed that the expression of Gb3S promoted the proliferation and migration of osteoblasts, which accelerated bone wound healing.