2009 Fiscal Year Final Research Report
Hypoxic stress in sleep apnea causes systemic inflammation and promotes atherosclerosis.
| Project/Area Number |
19390226
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Nara Medical University |
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Principal Investigator |
KIMURA Hiroshi Nara Medical University, 医学部, 教授 (20195374)
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| Co-Investigator(Kenkyū-buntansha) |
TAMAKI Shinji 奈良県立医科大学, 医学部, 助教 (30347546)
YAMAUCHI Motoo 奈良県立医科大学, 医学部, 助教 (30405378)
TOMODA Koichi 奈良県立医科大学, 医学部, 講師 (90364059)
YOSHIKAWA Masanori 奈良県立医科大学, 医学部, 准教授 (80271203)
HAMADA Kaoru 奈良県立医科大学, 医学部, 教授 (80228535)
MAKINODAN Kiyoshi 奈良県立医科大学, 医学部, 医員 (50382304)
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| Project Period (FY) |
2007 – 2009
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| Keywords | 睡眠時無呼吸 / 低酸素ストレス / 動脈硬化 / 単球 / 炎症性サイトカイン / アディポサイトカイン / 間歇的低酸素 / 内臓脂肪細胞 |
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| Research Abstract |
Obstructive sleep apnea syndrome (OSAS) is frequently associated with the complication of the cardiovascular diseases. However, the precise mechanism causing atherosclerosis has not been fully elucidated. We demonstrated that the productions of inflammatory mediators such as TNF-α and MCP-1 by monocytes were significantly elevated in OSAS patients as compared to in the control subjects. The invasive ability of monocytes evaluated by Matrigel Invasion Chamber was also significantly elevated in OSAS compared to in the control. Furthermore, we demonstrated the experimental exposure to intermittent hypoxia caused not only the increase in the production of inflammatory cytokines by monocytes, but also the decrease in the secretion of adipocytokines by visceral adipocytes of rats.
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