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Publication : RhoB deficiency in thymic medullary epithelium leads to early thymic atrophy.

First Author  Bravo-Nuevo A Year  2011
Journal  Int Immunol Volume  23
Issue  10 Pages  593-600
PubMed ID  21865151 Mgi Jnum  J:176422
Mgi Id  MGI:5291839 Doi  10.1093/intimm/dxr064
Citation  Bravo-Nuevo A, et al. (2011) RhoB deficiency in thymic medullary epithelium leads to early thymic atrophy. Int Immunol 23(10):593-600
abstractText  RhoB, a member of the Rho subfamily of small GTPases, mediates diverse cellular functions, including cytoskeletal organization, cell transformation and vesicle trafficking. The thymus undergoes progressive decline in its structure and function after puberty. We found that RhoB was expressed in thymic medullary epithelium. To investigate a role of RhoB in the regulation of thymic epithelial organization or thymocyte development, we analyzed the thymi of RhoB-deficient mice. RhoB-deficient mice were found to display earlier thymic atrophy. RhoB deficiency showed significant reductions in thymus weight and cellularity, beginning as early as 5 weeks of age. The enhanced expression of TGF-beta receptor type II (TGFbetaRII) in thymic medullary epithelium was observed in RhoB-null mice. In addition, the expression of fibronectin, which is shown to be regulated by TGF-beta signaling, was accordingly increased in the mutant thymic medulla. Since there is no age-related change of RhoB expression in the thymus, it is unlikely that RhoB in thymic epithelium directly contributes to age-related thymic involution. Nevertheless, our findings strongly support a physiological role of RhoB in regulation of thymus development and maintenance through the inhibition of TGF-beta signaling in thymic medullary epithelium.
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