| Project/Area Number |
25461194
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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 |
Respiratory organ internal medicine
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
Kuroki Yoshio 札幌医科大学, 医学部, 教授 (70161784)
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| Co-Investigator(Renkei-kenkyūsha) |
TAKAHASHI MOTOKO 札幌医科大学, 医学部, 准教授 (00303941)
ARIKI SHIGERU 札幌医科大学, 医学部, 准教授 (80464478)
HASEGAWA YOSHIHIRO 札幌医科大学, 医学部, 助教 (90643180)
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| Research Collaborator |
TAKAMIYA RINA
UEHARA YASUAKI
SAITO ATSUSHI
TAKAHASHI HIROKI
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 肺サーファクタント / 肺コレクチン / EGFシグナル / ディフェンシン / アクロレイン / 肺がん / 肥満細胞 / コレクチン / 肺癌 / SP-D / EGF / EGFR / 肺腺がん |
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| Outline of Final Research Achievements |
Pulmonary surfactant proteins, SP-A and SP-D, suppress the growth and progression of lung cancer cells by attenuating the EGF signaling of EGFR phosphorylation and its downstream. SP-D interferes with the EGF binding to EGFR by binding to the high mannose type-sugar moieties of EGFR. SP-A binds to EGFR in a Ca2+-independent manner, indicating the different mechanism from that of SP-D. SP-A and its peptide (SAP01:Tyr161-Lys201) attenuate mast cell migration stimulated with hBD3 and weakened the accumulation of mast cells in the tracheas of asthma model rats. SP-A protein was modified by cigarette smoke extract (CSE) and acrolein containing in the cigarette smoke. The reduction of reactive thiol in the SP-A molecule and the addition of acrolein was observed. The modified SP-A exhibited the decreased ability to attenuate the E. coli growth.
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