Open Access

Bradykinin receptors and EphB2/EphrinB2 pathway in response to high glucose-induced osteoblast dysfunction and hyperglycemia-induced bone deterioration in mice

Corrigendum in: /10.3892/ijmm.2019.4091

  • Authors:
    • Min Wu
    • Wenting Ai
    • Lin Chen
    • Sihai Zhao
    • Enqi Liu
  • View Affiliations

  • Published online on: January 12, 2016     https://doi.org/10.3892/ijmm.2016.2457
  • Pages: 565-574
  • Copyright: © Wu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

This study was carried out in order to investigate bone dysfunction and the involvement of bradykinin receptors and the Eph/Ephrin signaling pathway in osteoblasts and in mice with diabetes-related osteoporosis in response to exposure to high glucose. Osteogenic transdifferentiation was inhibited when the osteoblasts were exposed to high glucose, and the expression levels of bone formation-related genes [Runx2 and alkaline phosphatase (ALP)] were decreased, while those of bone resorption-related genes [matrix metalloproteinase (MMP)9 and carbonic anhydrase II (CAII)] were increased. Moreover, the mRNA and protein expression levels of bradykinin receptor B1 (BK1R)/bradykinin receptor B2 (BK2R) and EphB2/EphrinB2 were significantly decreased in the osteoblasts following exposure to high glucose. Intriguingly, the interaction between BK2R and EphB2/EphrinB2 was confirmed, and BK2R loss-of-function significantly decreased the mRNA and protein expression levels of EphB2/EphrinB4. In vivo, hyperglycemia induced the disequilibrium of calcium homeostasis through the inhibition of bone formation and the acceleration of bone resorption, which was manifested by the reduction of trabecular bone mass of the primary and secondary spongiosa, as well as by the increase in the number of mature osteoclasts throughout the proximal tibial metaphysis in mice with diabetes-related osteoporosis. Furthermore, the mRNA and protein expression levels of BK1R/BK2R and EphB2/EphrinB2 in the tibias of the mice with diabetes-related osteoporosis were significantly decreased. These results demonstrate that bradykinin receptors and the EphB4/EphrinB2 pathway mediate the development of complications in mice with diabetes-related osteoporosis and suggest that the inactivation of bradykinin receptors and the EphB4/EphrinB2 pathway enhance the severity of complications in mice with diabetes-related osteoporosis.
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March-2016
Volume 37 Issue 3

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Wu M, Ai W, Chen L, Zhao S and Liu E: Bradykinin receptors and EphB2/EphrinB2 pathway in response to high glucose-induced osteoblast dysfunction and hyperglycemia-induced bone deterioration in mice Corrigendum in /10.3892/ijmm.2019.4091. Int J Mol Med 37: 565-574, 2016.
APA
Wu, M., Ai, W., Chen, L., Zhao, S., & Liu, E. (2016). Bradykinin receptors and EphB2/EphrinB2 pathway in response to high glucose-induced osteoblast dysfunction and hyperglycemia-induced bone deterioration in mice Corrigendum in /10.3892/ijmm.2019.4091. International Journal of Molecular Medicine, 37, 565-574. https://doi.org/10.3892/ijmm.2016.2457
MLA
Wu, M., Ai, W., Chen, L., Zhao, S., Liu, E."Bradykinin receptors and EphB2/EphrinB2 pathway in response to high glucose-induced osteoblast dysfunction and hyperglycemia-induced bone deterioration in mice Corrigendum in /10.3892/ijmm.2019.4091". International Journal of Molecular Medicine 37.3 (2016): 565-574.
Chicago
Wu, M., Ai, W., Chen, L., Zhao, S., Liu, E."Bradykinin receptors and EphB2/EphrinB2 pathway in response to high glucose-induced osteoblast dysfunction and hyperglycemia-induced bone deterioration in mice Corrigendum in /10.3892/ijmm.2019.4091". International Journal of Molecular Medicine 37, no. 3 (2016): 565-574. https://doi.org/10.3892/ijmm.2016.2457