Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 226, Issue 1, Pages 110-121Publisher
WILEY
DOI: 10.1002/jcp.22311
Keywords
-
Categories
Funding
- NIH [HL54269]
- Biosystems Dynamics Summer Institute through an HHMI
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R15HL054269] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Fluid shear stress (FSS) exerted on endothelial cell (EC) surfaces induces actin cytoskeleton remodeling through mechanotransduction. This study was designed to determine whether FSS activates Jun N-terminal kinase (JNK), to examine the spatial and temporal distribution of active JNK relative to the actin cytoskeleton in ECs exposed to different FSS conditions, and to evaluate the effects of active JNK on actin realignment. Exposure to 15 and 20 dyn/cm(2) FSS induced higher activity levels of JNK than the lower 2 and 4 dyn/cm(2) flow conditions. At the higher FSS treatments, JNK activity increased with increasing exposure time, peaking 30 min after flow onset with an eightfold activity increase compared to cells in static culture. FSS-induced phospho-JNK co-localized with actin filaments at cell peripheries, as well as with stress fibers. Pharmacologically blocking JNK activity altered FSS-induced actin structure and distribution as a response to FSS. Our results indicate that FSS-induced actin remodeling occurs in three phases, and that JNK plays a role in at least one, suggesting that this kinase activity is involved in mechanotransduction from the apical surface to the actin cytoskeleton in ECs. J. Cell. Physiol. 226: 110-121, 2010. (C) 2010 Wiley-Liss, Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available