S100A4 regulates macrophage chemotaxis.
S100A4 regulates macrophage chemotaxis.
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DOI:
10.1091/mbc.e09-07-0609
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发表时间:
2010-08-01
影响因子:
3.3
通讯作者:
Bresnick AR
中科院分区:
文献类型:
--
作者:
Li ZH;Dulyaninova NG;House RP;Almo SC;Bresnick AR
Using a targeted genetic deletion, we show that the S100A4 metastasis factor is required for macrophage recruitment to sites of inflammation in vivo. S100A4−/− primary macrophages display defects in chemotaxis due to myosin-IIA overassembly and altered CSF-1 receptor signaling. These studies establish S100A4 as a regulator of macrophage motility. S100A4, a member of the S100 family of Ca2+-binding proteins, is directly involved in tumor metastasis. In addition to its expression in tumor cells, S100A4 is expressed in normal cells and tissues, including fibroblasts and cells of the immune system. To examine the contribution of S100A4 to normal physiology, we established S100A4-deficient mice by gene targeting. Homozygous S100A4−/− mice are fertile, grow normally and exhibit no overt abnormalities; however, the loss of S100A4 results in impaired recruitment of macrophages to sites of inflammation in vivo. Consistent with these observations, primary bone marrow macrophages (BMMs) derived from S100A4−/− mice display defects in chemotactic motility in vitro. S100A4−/− BMMs form unstable protrusions, overassemble myosin-IIA, and exhibit altered colony-stimulating factor-1 receptor signaling. These studies establish S100A4 as a regulator of physiological macrophage motility and demonstrate that S100A4 mediates macrophage recruitment and chemotaxis in vivo.
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影响因子:
20.3
作者:
Hatch, WC;Ganju, RK;Groopman, JE
通讯作者:
Groopman, JE
影响因子:
4.8
作者:
Brinson, AE;Harding, T;Graves, LM
通讯作者:
Graves, LM
影响因子:
11.2
作者:
Grum-Schwensen, B;Klingelhofer, J;Ambartsumian, N
通讯作者:
Ambartsumian, N
DOI:
10.1083/jcb.200212082
发表时间:
2003-08-04
期刊:
The Journal of cell biology
影响因子:
--
作者:
Faccio R;Novack DV;Zallone A;Ross FP;Teitelbaum SL
通讯作者:
Teitelbaum SL
影响因子:
7.3
作者:
Davies, BR;O'Donnell, M;Mellon, JK
通讯作者:
Mellon, JK