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JRM Vol.19 No.5 pp. 557-564
doi: 10.20965/jrm.2007.p0557
(2007)

Paper:

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Effect of Mechanical Environment of Focal Adhesions on Remodeling of Endothelial Cells Subjected to Cyclic Stretching Using Microsubstrates

Naoya Sakamoto, Yoshimasa Yamazaki, Toshiro Ohashi,
and Masaaki Sato

Department of Bioengineering and Robotics, Graduate School of Engineering, Tohoku University, 6-6-01 Aoba-yama, Sendai 980-8579, Japan

Received:
March 27, 2007
Accepted:
July 4, 2007
Published:
October 20, 2007
Creative Commons License
Keywords:
cyclic stretching, endothelial cells, micropillar substrate, focal adhesions, actin stress fibers
Abstract
Endothelial cells (ECs) adapt to mechanical environments such as cyclic stretching by altering their morphology and cytoskeletal structure. The detailed mechanism underlying EC remodeling in response to cyclic stretching, however, remains unclear. To understand the contribution of strain in contact area between focal adhesions (FAs) and the substrate to morphological and cytoskeletal changes in cells, we applied cyclic stretching to ECs using a microsubstrate with arrays of micropillars on which cells were selectively stretched between FAs but FA-substrate contact area were hardly stretched. Bovine aortic ECs were seeded on a silicone elastomer micropillar substrate in a silicone chamber. ECs were then subjected to 20% stretching at 0.5 Hz for up to 6 h using a stretching apparatus. Cells stretched on a flat substrate were also observed. Under static conditions, no significant difference was seen in EC morphology between flat and micropillar substrates. After exposure to cyclic stretching for 3 h, ECs on both flat and micropillar substrates were aligned perpendicular to the direction of stretching. Stress fibers were oriented about 60° to the direction of stretching on the flat substrate, while stress fibers were not aligned in any direction for the micropillar substrate. After 6 h of stretching, stress fibers on the micropillar substrate were oriented approximately 90° to the direction of stretching. These results suggest that strain in contact area between FAs and the substrate may have an impact on reorientation rates of stress fibers in ECs in response to cyclic stretching.
Cite this article as:
N. Sakamoto, Y. Yamazaki, T. Ohashi, and M. Sato, “Effect of Mechanical Environment of Focal Adhesions on Remodeling of Endothelial Cells Subjected to Cyclic Stretching Using Microsubstrates,” J. Robot. Mechatron., Vol.19 No.5, pp. 557-564, 2007.
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References
  1. [1] P. F. Davis, “Flow-Medicated Endothelial Mechanotransduction,” Physiol. Rev., Vol.75, pp. 519-560, 1995.
  2. [2] A. M. Makek, S. L. Alper, and S. Izumo, “Hemodynamic Shear Stress an its Role in Atherosclerosis,” JAMA, Vol.285, pp. 2035-2042, 1999.
  3. [3] T. Takemasa, T. Yamaguchi, Y. Yamamoto, K. Sugimoto, and K. Yamashita, “Oblique Alignment of Stress Fibers in Cells Reduces the Mechanical Stress in Cyclically Deforming Fields,” Eur. J. Cell Biol., Vol.77, pp. 91-99, 1998.
  4. [4] H. C. Wang, W. I. Ip, R. Boissy, and E. S. Grood, “Cell Orientation Response to Cyclically Deformed Substrates: Experimental Validation of a Cell Model,” J. Biomech., Vol.7, pp. 130-138, 1995.
  5. [5] J. H. Wang, “Substrate Deformation Determines Actin Cytoskeleton Reorganization: A Mathematical Modeling and Experimental Study,” J. Theor. Biol., Vol.202, pp. 33-41, 2000.
  6. [6] H. Yamada, T. Takemasa, and T. Yamaguchi, “Theoretical Study of Intracellular Stress Fiber Orientation Under Cyclic Deformation,” J. Biomech., Vol.33, pp. 1501-1505, 2000.
  7. [7] S. K. Sastery and K. Burridge, “Focal Adhesions: A Nexus for Intracellular Signaling and Cytoskeletal Dyamics,” Exp. Cell Res., Vol.261, pp. 25-36, 2000.
  8. [8] P. Girard and R. M. Nerem, “Shear Stress Modulates Endothelial Cell Morphology and F-Actin Organization Through the Regulation of Focal Adhesion-Associated Proteins,” J. Cell. Physiol., Vol.163, pp. 179-193, 1995.
  9. [9] Y. Shikata, A. Rios, K. Kawkitinarong, N. DePaola, J. G. N. Garcia, and K. G. Birukov, “Differential Effects of Shear Stress and Cyclic Stretch on Focal Adhesion Remodeling, Site-Specific FAK Phosphorylation, and Small GTPases in Human Lung Endothelial Cells,” Exp. Cell Res., Vol.304, pp. 40-49, 2005.
  10. [10] M. R. Mofrad, N. A. Abdul-Rahim, H. Karcher, P. J. Mack, B. Yap, and R. D. Kamm, “Exploring the Molecular Basis for Mechanosensation, Signal Transduction, and Cytoskeletal Remodeling,” Acta Biomater., Vol.1, pp. 281-293, 2005.
  11. [11] D. Lehnert, B. Wehrle-Haller, C. David, U. Weiland, C. Ballestem, B. A. Imhof, and M. Bastmeyer, “Cell Behaviour on Micropatterned Substrata: Limits of Extracellular Matix Geometry for Spreading Adhesion,” J. Cell Sci., Vol.117, pp. 41-52, 2004.
  12. [12] J. M. Goffin, P. Pittet, G. Csucs, J. W. Lussi, J. J. Meister, and B. Hinz, “Focal Adhesion Size Controls Tension-Dependent Recruitment of α-Smooth Muscle actin to Stress Fibers,” J. Cell Biol., Vol.172, pp. 259-268, 2006.
  13. [13] T. Takemasa, K. Sugimoto, and K. Yamashita, “Amplitude-Dependent Stress Fiber Reorientation in Early Response to Cyclic Stretch,” Exp. Cell Res., Vol.230, pp. 407-410, 1997.
  14. [14] K. Naruse, T. Yamada, and M. Sokabe, “Involvement of SA Channels in Orienting Response of Cultured Endothelial Cells to Cyclic Stretch,” Am. J. Physiol., Vol.274, pp. H1532-H1538, 1998.
  15. [15] J. H. Wang, P. Goldschmidt-Clermont, J. Wille, and F. C. Yin, “Specificity of Endothelial Cell Reorientation in Response to Cyclic Mechanical Stretching,” J. Biomech., Vol.34, pp. 1563-1572, 2001.
  16. [16] A. D. Bershadskey, C. Ballestrem, L. Carramusa, Y. Ziberman, B. Gilquin, S. Khochbin, A. Y. Alexandrove, A. B. Verkhovsky, T. Shemesh, and M. M. Kozlov, “Assembly and Mechanosensory Function of Focal Adhesions: Experimental and Models,” Eur. J. Cell Biol., Vol.85, pp. 165-173, 2000.
  17. [17] A. E. Aplin, A. Howe, S. K. Alahari, and R. L. Juliano, “Signal Transduction and Signal Modulation by Cell Adhesion Receptors: The Role of Integrins, Cadherins, Immunogloblin-Cell Adhesion Molecules, and Selectins,” Pharmacol. Rev., Vol.50, pp. 197-263, 1998.
  18. [18] B.-H. Luo and T. A. Springer, “Integrin Structure and Conformational Signaling,” Curr. Opin. Cell Biol., Vol.18, pp. 579-586, 2006.
  19. [19] M. Thèry, A. Pèpin, E. Dressaire, Y. Chen, and M. Bronens, “Cell Distribution of Stress Fibres in Response to the Geometry of the Adhesive Environment,” CellMotil. Cytoskel., Vol.63, pp. 341-355, 2006.
  20. [20] J. L. Tan, J. Tein, D. M. Pirone, D. S. Gray, K. Bhadriraju, and C. S. Chen, “Cells Lying on a Bed of Microneedles: An Approach to Isolate Mechanical Force,” PNAS, Vol.100, pp. 1484-1489, 2003.
  21. [21] C. S. Chen, J. L. Alonso, E. Ostuni, G. M. Whitesides, and D. E. Ingber, “Cell Shape Provides Global Control of Focal Adhesion Assembly,” Biochem. Biophys. Res. Comm., Vol.307, pp. 355-361, 2003.
  22. [22] F. S. M. Ismail, R. Rohanizadeh, S. Atwa, R. S.,Mason, A. J. Ruys, P. J. Matin, and A. Bendavid, “The influence of Surface Chemistry and Topography on the Contact Guidance of MG63 Osteoblast Cells,” J. Mater. Sci.: Mater. Med., Vol.18, pp. 705-714, 2007.

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