Annexin 1 modulates monocyte-endothelial cell interaction in vitro and cell migration in vivo in the human SCID mouse transplantation model.
Annexin 1 modulates monocyte-endothelial cell interaction in vitro and cell migration in vivo in the human SCID mouse transplantation model.
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DOI：
10.4049/jimmunol.169.4.2085
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发表时间：
2002-08-15
期刊：
影响因子：
--
通讯作者：
Pitzalis C
中科院分区：
文献类型：
--
作者：
Perretti M;Ingegnoli F;Wheller SK;Blades MC;Solito E;Pitzalis C
通过转染表达不同蛋白水平的U937细胞，研究糖皮质激素诱导蛋白annexin 1 （ANXA1）对单核细胞迁移过程的影响。获得了一个反义（AS） （34.1 AS，约50%的ANXA1）和一个义(S)克隆（15S，过表达生物活性24kda片段）以及空质粒CMV克隆，并与野生型U937细胞进行了体外和体内各种细胞迁移模型的比较。15s转染的U937细胞在基质细胞衍生因子-1α （CXC趋化因子配体12 (CXCL12)）的作用下，显示出跨内皮迁移程度降低（50%）。此外，内源性ANXA1对体外U937细胞迁移的抑制作用通过中和性抗ANXA1血清的增强作用得到证实。重要的是，克隆15S中ANXA1的过表达抑制了移植到SCID小鼠的类风湿性滑膜移植物的细胞迁移程度。从转染和野生型U937细胞中发现的相似数量的表面分子可以看出，ANXA1的抑制作用不是由于粘附分子或CXCL12受体（CXCR4）表达的改变。同样，体外对CXCL12的相同趋化反应排除了克隆15S和36.4AS中细胞运动的内在缺陷。这些数据有力地支持了这样一种观点，即ANXA1严重干扰了U937细胞（可能还有单核细胞）在体外和体内迁移所必需的白细胞内皮步骤。
The effect of the glucocorticoid inducible protein annexin 1 (ANXA1) on the process of monocytic cell migration was studied using transfected U937 cells expressing variable protein levels. An antisense (AS) (36.4AS; ~50% less ANXA1) and a sense (S) clone (15S; overexpressing the bioactive 24-kDa fragment) together with the empty plasmid CMV clone were obtained and compared with wild-type U937 cells in various models of cell migration in vitro and in vivo. 15S-transfected U937 cells displayed a reduced (50%) degree of trans-endothelial migration in response to stromal cell-derived factor-1α (CXC chemokine ligand 12 (CXCL12)). In addition, the inhibitory role of endogenous ANXA1 on U937 cell migration in vitro was confirmed by the potentiating effect of a neutralizing anti-ANXA1 serum. Importantly, overexpression of ANXA1 in clone 15S inhibited the extent of cell migration into rheumatoid synovial grafts transplanted into SCID mice. ANXA1 inhibitory effects were not due to modifications in adhesion molecule or CXCL12 receptor (CXCR4) expression as shown by the similar amounts of surface molecules found in transfected and wild-type U937 cells. Likewise, an equal chemotactic response to CXCL12 in vitro excluded an intrinsic defect in cell motility in clones 15S and 36.4AS. These data strongly support the notion that ANXA1 critically interferes with a leukocyte endothelial step essential for U937 cell, and possibly monocyte, transmigration both in vitro and in vivo.
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DOI：
10.1073/pnas.95.24.14535
发表时间：
1998-11-24
影响因子：
11.1
作者：
Lim, LHK;Solito, E;Perretti, M
通讯作者：
Perretti, M
影响因子：
5.5
作者：
HOFF, T;SPENCKER, T;GOPPELTSTRUEBE, M
通讯作者：
GOPPELTSTRUEBE, M
DOI：
10.1152/ajpheart.1994.267.4.h1573
发表时间：
1994-10-01
影响因子：
4.8
作者：
BIENVENU, K;HARRIS, N;GRANGER, DN
通讯作者：
GRANGER, DN
影响因子：
5.5
作者：
CAVENDER, DE;EDELBAUM, D;WELKOVICH, L
通讯作者：
WELKOVICH, L
影响因子：
--
作者：
Blades, MC;Ingegnoli, F;Pitzalis, C
通讯作者：
Pitzalis, C