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BOR - Papers in Press, published online ahead of print December 15, 2004.
Biol Reprod 2004, 10.1095/biolreprod.104.035089
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BIOLOGY OF REPRODUCTION 72, 916–921 (2005)
DOI: 10.1095/biolreprod.104.035089
© 2005 by the Society for the Study of Reproduction, Inc.

Establishment of Penile Fibrosis Model in a Rat Using Mouse NIH 3T3 Fibroblasts Expressing Transforming Growth Factor ß11

Ji-Kan Ryu3, Sun U. Song4, Jee-Young Han5, Young-Chae Chu5, Minhyung Lee4, Jun-Sig Kim6, Seong-Jin Kim7, and Jun-Kyu Suh2,3

Departments of Urology,3 Clinical Research Center,4 Pathology,5 Emergency Medicine,6 Inha University Collegeof Medicine, Incheon 400-103, South Korea Laboratory of Cell Regulation and Carcinogenesis,7 National Cancer Institute, Bethesda, Maryland 20892-5055

Transforming growth factor (TGF) ß1 has been suggested to have an important role in cavernous fibrosis and resultant erectile dysfunction. For further elucidation of TGFß1 signaling in association with cavernous fibrosis, we developed a rat model of cavernous fibrosis using TGFß1-producing NIH 3T3 fibroblasts (NIH 3T3-TGFß1). The NIH 3T3-TGFß1 cells were injected into male Sprague-Dawley rats intracavernously. Masson trichrome staining at 20 days postinjection showed multiple fibrous scars in the rats injected with the NIH 3T3-TGFß1 cells (group 3), whereas no histological evidence of cavernous fibrosis was found in the control rats (group 1) or the recombinant human TGFß1 protein-injected rats (group 2). Immunohistochemical staining revealed a higher expression of TGFß1 and its type II receptor in group 3 than in groups 1 and 2. Electrostimulation of the cavernous nerve revealed that the maximal intracavernous pressure was significantly lower in group 3 than in groups 1 and 2 (P < 0.01). The expression of transgenic TGFß1 mRNA continued to 10 days after injection of the cells. The NIH 3T3-TGFß1 cells sufficiently induced relatively long-lasting cavernous fibrosis. This novel animal model may contribute to future investigations of the pathogenesis of penile fibrosis associated with TGFß1 signaling and the development of new therapeutics targeting this pathway.

1 Supported by Grant R01-2002-000-00009-0 (2002) from the Basic Research Program of the Korea Science and Engineering Foundation.

2 Correspondence: Jun-Kyu Suh, Department of Urology, Inha University Hospital, 7-206 Third St., Shinheung-Dong, Jung-Gu, Incheon 400-103, South Korea. FAX: 82 32 890 2363; jksuh{at}inha.ac.kr






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Copyright © 2005 by the Society for the Study of Reproduction.