A2B Adenosine Receptor Stimulation Down-regulates M-CSF-mediated Osteoclast ProliferationA2B Adenosine Receptor Stimulation Down-regulates M-CSF-mediated Osteoclast Proliferation
- Other Titles
- A2B Adenosine Receptor Stimulation Down-regulates M-CSF-mediated Osteoclast Proliferation
- Authors
- 오윤택; 이나경
- Issue Date
- 2017
- Publisher
- 대한의생명과학회
- Keywords
- M-CSF; Osteoclast proliferation; A2B adenosine receptor; Akt
- Citation
- 대한의생명과학회지, v.23, no.3, pp.194 - 200
- Journal Title
- 대한의생명과학회지
- Volume
- 23
- Number
- 3
- Start Page
- 194
- End Page
- 200
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/8128
- DOI
- 10.15616/BSL.2017.23.3.194
- Abstract
- Bone-resorbing osteoclasts play a major role in maintaining bone homeostasis with bone-forming osteoblasts.
Although it has been reported that A2B adenosine receptor (A2BAR) regulates osteoclast differentiation, its effects on apoptosis or proliferation of osteoclasts have been less-defined. Here, we demonstrate that A2BAR stimulation regulates macrophage-colony stimulating factor (M-CSF)-mediated osteoclast proliferation. Stimulation with a specific agonist of A2BAR, BAY 60-6583, significantly reduced M-CSF-mediated osteoclast proliferation in a time- and dose-dependent manner. In addition, A2BAR stimulation induced both apoptosis of the cells and cell arrest in the G1 phase with a decrease of cell number in the G2/M phase. Stimulation with BAY 60-6583 inhibited the activation of Akt by M-CSF, whereas M-CSF-induced ERK1/2 activation was not affected. These results suggest that the inhibition of M-CSF-mediated Akt activation by A2BAR stimulation increases apoptotic response of osteoclasts and induces cell cycle arrest in the G1 phase, thus contributing to the down-regulation of osteoclast proliferation.
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Collections - College of Medical Sciences > Department of Biomedical Laboratory Science > 1. Journal Articles
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