The Role of Src Kinase inMacrophage-Mediated Inflammatory Responses

被引:200
作者
Byeon, Se Eun [1 ]
Yi, Young-Su [1 ]
Oh, Jueun [1 ]
Yoo, Byong Chul [2 ]
Hong, Sungyoul [1 ]
Cho, Jae Youl [1 ]
机构
[1] Sungkyunkwan Univ, Dept Genet Engn, Suwon 446746, South Korea
[2] Res Inst & Hosp, Natl Canc Ctr, Goyang 410769, South Korea
基金
新加坡国家研究基金会;
关键词
PROTEIN-TYROSINE KINASES; NF-KAPPA-B; FC-GAMMA-RII; TNF-ALPHA PRODUCTION; C-SRC; FAMILY KINASES; KUPFFER CELLS; SIGNAL-TRANSDUCTION; LIPOTEICHOIC ACID; ETHANOL EXTRACT;
D O I
10.1155/2012/512926
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Src kinase (Src) is a tyrosine protein kinase that regulates cellular metabolism, survival, and proliferation. Many studies have shown that Src plays multiple roles in macrophage-mediated innate immunity, such as phagocytosis, the production of inflammatory cytokines/mediators, and the induction of cellular migration, which strongly implies that Src plays a pivotal role in the functional activation of macrophages. Macrophages are involved in a variety of immune responses and in inflammatory diseases including rheumatoid arthritis, atherosclerosis, diabetes, obesity, cancer, and osteoporosis. Previous studies have suggested roles for Src in macrophage-mediated inflammatory responses; however, recently, new functions for Src have been reported, implying that Src functions in macrophage-mediated inflammatory responses that have not been described. In this paper, we discuss recent studies regarding a number of these newly defined functions of Src in macrophage-mediated inflammatory responses. Moreover, we discuss the feasibility of Src as a target for the development of new pharmaceutical drugs to treat macrophage-mediated inflammatory diseases. We provide insights into recent reports regarding new functions for Src that are related to macrophage-related inflammatory responses and the development of novel Src inhibitors with strong immunosuppressive and anti-inflammatory properties, which could be applied to various macrophage-mediated inflammatory diseases.
引用
收藏
页数:18
相关论文
共 163 条
[1]   NADPH oxidase activity is required for endothelial cell proliferation and migration [J].
Abid, MR ;
Kachra, Z ;
Spokes, KC ;
Aird, WC .
FEBS LETTERS, 2000, 486 (03) :252-256
[2]   Pseudomonas aeruginosa flagella activate airway epithelial cells through asialoGM1 and toll-like receptor 2 as well as toll-like receptor 5 [J].
Adamo, R ;
Sokol, S ;
Soong, G ;
Gomez, MI ;
Prince, A .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2004, 30 (05) :627-634
[3]  
ANDERSON SM, 1990, ONCOGENE, V5, P317
[4]   Receptor-mediated tobacco toxicity:: acceleration of sequential expression of α5 and α7 nicotinic receptor subunits in oral keratinocytes exposed to cigarette smoke [J].
Arredondo, Juan ;
Chernyavsky, Alexander I. ;
Jolkovsky, David L. ;
Pinkerton, Kent E. ;
Grando, Sergei A. .
FASEB JOURNAL, 2008, 22 (05) :1356-1368
[5]   Development of T-leukaemias in CD45 tyrosine phosphatase-deficient mutant lck mice [J].
Baker, M ;
Gamble, J ;
Tooze, R ;
Higgins, D ;
Yang, FT ;
O'Brien, PCM ;
Coleman, N ;
Pingel, S ;
Turner, M ;
Alexander, DR .
EMBO JOURNAL, 2000, 19 (17) :4644-4654
[6]   MYC BUT NOT FOS RESCUE OF PDGF SIGNALING BLOCK CAUSED BY KINASE INACTIVE SRC [J].
BARONE, MV ;
COURTNEIDGE, S .
NATURE, 1995, 378 (6556) :509-512
[7]  
Bewarder N, 1996, MOL CELL BIOL, V16, P4735
[8]  
Billiar T. R., 1990, J PARENTERAL ENTERAL, V14
[9]  
BILLIAR TR, 1989, ARCH SURG-CHICAGO, V124, P1416
[10]   Identification of protein-tyrosine phosphatase 1B as the major tyrosine phosphatase activity capable of dephosphorylating and activating c-Src in several human breast cancer cell lines [J].
Bjorge, JD ;
Pang, A ;
Fujita, DJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (52) :41439-41446