This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nakao, N. Articles by Kusakabe, M. Search for Related Content PubMed PubMed Citation Articles by Nakao, N. Articles by Kusakabe, M.

American Journal of Pathology, Vol 152, 1237-1245, Copyright © 1998 by American Society for Investigative Pathology

REGULAR ARTICLES

Tenascin-C promotes healing of Habu-snake venom-induced glomerulonephritis: studies in knockout congenic mice and in culture

N Nakao, N Hiraiwa, A Yoshiki, F Ike and M Kusakabe
Renal Division, Internal Medicine, GenGen do-Kimitu Hospital, Chiba, Japan.

Mice without the gene for tenascin-C, a multifunctional extracellular matrix protein expressed in many important biological events, including wound healing, did not show any phenotype. However, it is now obvious that the phenotype of deletion of one gene frequently depends on the genetic background. Therefore, we have newly generated tenascin-C knockout mice (KO) by backcrossing original KO into three congenic lines: C57BL/6N, BALB/cA, and GRS/A (GR). And we investigated the disease course of reversible kidney injury, Habu-snake venom-induced proliferative glomerulonephritis. In all strains, the disease was more severe in KO, but the severity varied with the strain. The KO-GR showed irreversibility; all treated KO-GR died by the 4th month due to renal failure. The diseased KO-GR showed abnormal regenerative reactions, including reduced proliferation of mesangial cells, key players in glomerulonephritis, and reduced production of some kinds of cytokines and matrices, leading to poor formation of granulation tissue. In culture, the mesangial cells from the KO-GR had the same potential for proliferation and response to cytokines as controls, but interestingly, to achieve this potential, they required contact with tenascin-C. These reactions were blocked by an anti-tenascin monoclonal antibody. The results of the present study, the first report showing the most dramatic phenotype so far discovered, have strongly suggested the importance of tenascin-C in the resolution of the renal inflammation and that of the genetic background on which the KO was developed.

This article has been cited by other articles:

				A. Matsuda, T. Hirota, M. Akahoshi, M. Shimizu, M. Tamari, A. Miyatake, A. Takahashi, K. Nakashima, N. Takahashi, K. Obara, et al. Coding SNP in tenascin-C Fn-III-D domain associates with adult asthma Hum. Mol. Genet., October 1, 2005; 14(19): 2779 - 2786. [Abstract] [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]

				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]

				S. V. Griffin, K. Hiromura, J. Pippin, A. T. Petermann, M. J. Blonski, R. Krofft, S. Takahashi, A. B. Kulkarni, and S. J. Shankland Cyclin-Dependent Kinase 5 Is a Regulator of Podocyte Differentiation, Proliferation, and Morphology Am. J. Pathol., October 1, 2004; 165(4): 1175 - 1185. [Abstract] [Full Text] [PDF]

				A. Hartner, N. Cordasic, B. Klanke, R. Veelken, and K. F. Hilgers Strain differences in the development of hypertension and glomerular lesions induced by deoxycorticosterone acetate salt in mice Nephrol. Dial. Transplant., October 1, 2003; 18(10): 1999 - 2004. [Abstract] [Full Text] [PDF]

				M. D. Puente Navazo, D. Valmori, and C. Ruegg The Alternatively Spliced Domain TnFnIII A1A2 of the Extracellular Matrix Protein Tenascin-C Suppresses Activation-Induced T Lymphocyte Proliferation and Cytokine Production J. Immunol., December 1, 2001; 167(11): 6431 - 6440. [Abstract] [Full Text] [PDF]

				E. Garcion, A. Faissner, and C. ffrench-Constant Knockout mice reveal a contribution of the extracellular matrix molecule tenascin-C to neural precursor proliferation and migration Development, July 1, 2001; 128(13): 2485 - 2496. [Abstract] [Full Text] [PDF]

				R. Raballo, J. Rhee, R. Lyn-Cook, J. F. Leckman, M. L. Schwartz, and F. M. Vaccarino Basic Fibroblast Growth Factor (Fgf2) Is Necessary for Cell Proliferation and Neurogenesis in the Developing Cerebral Cortex J. Neurosci., July 1, 2000; 20(13): 5012 - 5023. [Abstract] [Full Text] [PDF]

				D. KOYA, M. HANEDA, H. NAKAGAWA, K. ISSHIKI, H. SATO, S. MAEDA, T. SUGIMOTO, H. YASUDA, A. KASHIWAGI, D. K. WAYS, et al. Amelioration of accelerated diabetic mesangial expansion by treatment with a PKC {beta} inhibitor in diabetic db/db mice, a rodent model for type 2 diabetes FASEB J, March 1, 2000; 14(3): 439 - 447. [Abstract] [Full Text]

				G. Tononi, O. Sporns, and G. M. Edelman Measures of degeneracy and redundancy in biological networks PNAS, March 16, 1999; 96(6): 3257 - 3262. [Abstract] [Full Text] [PDF]

				E. Mackie and R. Tucker The tenascin-C knockout revisited J. Cell Sci., January 11, 1999; 112(22): 3847 - 3853. [Abstract] [PDF]