2015 Fiscal Year Final Research Report
Molecular insights of the crosstalk between locomotive and metabolic syndromes
| Project/Area Number |
25462380
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Saitama Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKACHI YUTAKA 埼玉医科大, 医学部, 助教 (10522097)
SUDA TATSUO 埼玉医科大, 医学部, 客員教授 (90014034)
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| Co-Investigator(Renkei-kenkyūsha) |
SUGAHARA IZUMI 埼玉医科大, 医学部, 研究員 (10633000)
OKAZAKI YASUSHI 埼玉医科大, 医学部, 教授 (80280733)
YASUNAMI YOICHI 福岡大学, 医学部, 教授 (00166521)
SATO TSUYOSHI 福岡大学, 医学部, 准教授 (60406494)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 骨代謝 / 糖代謝 / エピジェネティック / 転写因子 |
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| Outline of Final Research Achievements |
Elucidation of molecular insights underlying the crosstalk between metabolic and rocomotive syndromes is important since it is clearly shown that most of diabetic patients accompanies with vulnerability of their bones, resulting from the bone destruction. Herein we found several evidence as below. First, a transcription factor Pax6, is critical for pancreatic endocrine cell differentiation, attenuates the differentiation of osteoclasts. Second, a neuropeptide CRF suppresses apoptosis of pancreatic beta cells treated with inflammatory cytokines. Third, endothelial cell-derived Netrin-4 inhibits osteoclatogenesis. Lastly, the gene expression of a limited sets of cell cycle regulators mediated by DNA methylation might contribute to osteoblast differentiation. Control of Pax6 transcription and epigenetic functionality therefore may lead to explore and identify novel therapeutic targets upon unknown crosstalk essential for metabolic syndromes both of bone and glucose.
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| Free Research Field |
糖代謝、骨代謝、分子生物学
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