2020 Fiscal Year Annual Research Report
Elucidation of the molecular mechanisms for the impaired bone formation in disuse osteoporosis and GC-induced osteoporosis using Fkbp5 knockout mice
| Project/Area Number |
19K24124
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| Research Institution | Nagasaki University |
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Principal Investigator |
QIN XIN 長崎大学, 医歯薬学総合研究科(歯学系), 特任研究員 (60846559)
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| Project Period (FY) |
2019-08-30 – 2021-03-31
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| Keywords | osteoporosis / bone development |
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| Outline of Annual Research Achievements |
We identified Fkbp5 as an unloading-induced molecule in osteoblasts and osteocytes. We generated Fkbp5 knockout (Fkbp5KO) mice. Bone loss occurred more severely in Fkbp5 knockout mice than wild-type mice at unloading condition and with glucocorticoid (GC) treatment.
We collected RNA from the osteoblast-enriched fraction from wild-type and Fkbp5KO; mice with or without GC treatment. Osteoblast marker gene expressions were drastically reduced, Dex treatment reduces Runx2 protein level to nearly half in wild type mice and more severely in Fkbp5KO mice.
We performed microarray analysis by using osteoblast and osteocyte fractions. The expression of the selected genes by gene annotation and pathway analyses was analyzed by real-time reverse transcription (RT)-PCR.
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