The role of actin-binding protein 280 in integrin-dependent mechanoprotection

被引:208
作者
Glogauer, M
Arora, P
Chou, D
Janmey, PA
Downey, GP
McCulloch, CAG
机构
[1] Univ Toronto, Fac Dent, MRC, Periodontal Physiol Grp, Toronto, ON M5S 1A8, Canada
[2] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02115 USA
[3] Univ Toronto, Fac Med, Dept Med, Toronto, ON M5S 1A8, Canada
关键词
D O I
10.1074/jbc.273.3.1689
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
To survive in a mechanically active environment, cells must adapt to variations of applied membrane tension, A collagen-coated magnetic bead model was used to apply forces directly to the actin cytoskeleton through integrin receptors, We demonstrate here that by a calcium-dependent mechanism, human fibroblasts reinforce locally their connection with extracellular adhesion sites by inducing actin assembly and by recruiting actin-binding protein 280 (ABP-280) into cortical adhesion complexes, ABP-280 was phosphorylated on serine residues as a result of force application, This phosphorylation and the force-induced actin reorganization were largely abrogated by inhibitors of protein kinase C. In a human melanoma cell line that does not express ABP-280, actin accumulation could not be induced by force, whereas in stable transfectants expressing ABP-280, force-induced actin accumulation was similar to human fibroblasts, Cortical actin assembly played a role in regulating the activity of stretch-activated, calcium permeable channels (SAG) since sustained force application desensitized SAC to subsequent force applications, and the decrease in stretch sensitivity was reversed after treatment with cytochalasin D. ABP-280-deficient cells showed a >90% increase in cell death compared with ABP-280+ve cells after force application. We conclude that ABP-280 plays an important role in mechanoprotection by reinforcing the membrane cortex and desensitizing SACs.
引用
收藏
页码:1689 / 1698
页数:10
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