![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
|
|
|
|
|
||
A more recent version of this article appeared on October 1, 2002
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on December 19, 2001
Revised on May 20, 2002
Accepted on July 9, 2002
1 Department of Molecular Biology, Princeton University, Princeton, NJ 08544-1014
* Corresponding author. E-mail address: jschwarzbauer{at}molbio.princeton.edu.
A provisional matrix consisting of fibrin and fibronectin (FN) is deposited at sites of tissue damage and repair. This matrix serves as a scaffold for fibroblast migration into the wound where these cells deposit new matrix to replace lost or damaged tissue and eventually contract the matrix to bring the margins of the wound together. Tenascin-C is expressed transiently during wound repair in tissue adjacent to areas of injury and contacts the provisional matrix in vivo. Using a synthetic model of the provisional matrix, we have found that tenascin-C regulates cell responses to a fibrin-FN matrix through modulation of focal adhesion kinase (FAK) and RhoA activation. Cells on fibrin-FN+tenascin-C redistribute their actin to the cell cortex, down-regulate focal adhesion formation and do not assemble a FN matrix. Cells surrounded by a fibrin-FN+tenascin-C matrix are unable to induce matrix contraction. The inhibitory effect of tenascin-C is circumvented by downstream activation of RhoA. FAK is also required for matrix contraction and the absence of FAK cannot be overcome by activation of RhoA. These observations show dual requirements for both FAK and RhoA activities during contraction of a fibrin-FN matrix. The effects of tenascin-C combined with its location around the wound bed suggest that this protein regulates fundamental processes of tissue repair by limiting the extent of matrix deposition and contraction to fibrin-FN-rich matrix in the primary wound area.
This article has been cited by other articles:
|
|
 |
|
  A. Leask, X. Shi-wen, K. Khan, Y. Chen, A. Holmes, M. Eastwood, C. P. Denton, C. M. Black, and D. J. Abraham Loss of protein kinase C{epsilon} results in impaired cutaneous wound closure and myofibroblast function J. Cell Sci., October 15, 2008; 121(20): 3459 - 3467. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Liu, J. Lu, W. V. Cardoso, and C. Vaziri The SPARC-related Factor SMOC-2 Promotes Growth Factor-induced Cyclin D1 Expression and DNA Synthesis via Integrin-linked Kinase Mol. Biol. Cell, January 1, 2008; 19(1): 248 - 261. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Saito, H. Imazeki, S. Miura, T. Yoshimura, H. Okutsu, Y. Harada, T. Ohwaki, O. Nagao, S. Kamiya, R. Hayashi, et al. A Peptide Derived from Tenascin-C Induces 1 Integrin Activation through Syndecan-4 J. Biol. Chem., November 30, 2007; 282(48): 34929 - 34937. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. C. Yates, D. Whaley, P. Kulasekeran, W. W. Hancock, B. Lu, R. Bodnar, J. Newsome, P. A. Hebda, and A. Wells Delayed and Deficient Dermal Maturation in Mice Lacking the CXCR3 ELR-Negative CXC Chemokine Receptor Am. J. Pathol., August 1, 2007; 171(2): 484 - 495. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Lange, M. Kammerer, M. E. Hegi, S. Grotegut, A. Dittmann, W. Huang, E. Fluri, G. W. Yip, M. Gotte, C. Ruiz, et al. Endothelin Receptor Type B Counteracts Tenascin-C-Induced Endothelin Receptor Type A-Dependent Focal Adhesion and Actin Stress Fiber Disorganization Cancer Res., July 1, 2007; 67(13): 6163 - 6173. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. C. Hsia and J. E. Schwarzbauer Meet the Tenascins: Multifunctional and Mysterious J. Biol. Chem., July 22, 2005; 280(29): 26641 - 26644. [Full Text] [PDF]
|
|
|
|
|
|
M. Tamaoki, K. Imanaka-Yoshida, K. Yokoyama, T. Nishioka, H. Inada, M. Hiroe, T. Sakakura, and T. Yoshida Tenascin-C Regulates Recruitment of Myofibroblasts during Tissue Repair after Myocardial Injury Am. J. Pathol., July 1, 2005; 167(1): 71 - 80. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. J. Stevenson, A. Koncarevic, P. G. Giresi, R. W. Jackman, and S. C. Kandarian Transcriptional profile of a myotube starvation model of atrophy J Appl Physiol, April 1, 2005; 98(4): 1396 - 1406. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. S. Midwood, L. V. Valenick, H. C. Hsia, and J. E. Schwarzbauer Coregulation of Fibronectin Signaling and Matrix Contraction by Tenascin-C and Syndecan-4 Mol. Biol. Cell, December 1, 2004; 15(12): 5670 - 5677. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A Juuti, S Nordling, J Louhimo, J Lundin, and C Haglund Tenascin C expression is upregulated in pancreatic cancer and correlates with differentiation J. Clin. Pathol., November 1, 2004; 57(11): 1151 - 1155. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A. Wozniak, R. Desai, P. A. Solski, C. J. Der, and P. J. Keely ROCK-generated contractility regulates breast epithelial cell differentiation in response to the physical properties of a three-dimensional collagen matrix J. Cell Biol., November 10, 2003; 163(3): 583 - 595. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Wierzbicka-Patynowski and J. E. Schwarzbauer The ins and outs of fibronectin matrix assembly J. Cell Sci., August 15, 2003; 116(16): 3269 - 3276. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Filenius, T. Tervo, and I. Virtanen Production of Fibronectin and Tenascin Isoforms and Their Role in the Adhesion of Human Immortalized Corneal Epithelial Cells Invest. Ophthalmol. Vis. Sci., August 1, 2003; 44(8): 3317 - 3325. [Abstract] [Full Text] [PDF]
|
|
