Studies of pulmonary surfactant proteins on new aspects of host defense functions: anti-tumor activity and defensive activity against disease development.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461194
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Respiratory organ internal medicine
• Research Institution: Sapporo Medical University
• Principal Investigator: Kuroki Yoshio 札幌医科大学, 医学部, 教授 (70161784)
• 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)
• Research Collaborator: TAKAMIYA RINA ; UEHARA YASUAKI ; SAITO ATSUSHI ; TAKAHASHI HIROKI
• Project Period (FY): 2013-04-01 – 2016-03-31
• 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

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.

Free Research Field

医化学