The first two authors contributed equally to this work.
Immunohistochemical study of flotillin-1 in rat testis with ischemia/reperfusion injury
Article first published online: 2 JAN 2013
© The Author(s) Journal compilation © 2007 International Federation for Cell Biology
Cell Biology International
Volume 31, Issue 6, pages 609–614, June 2007
How to Cite
Jeong, C.-w., Kim, H., Kim, S., Kim, S.-H., Moon, C. and Shin, T. (2007), Immunohistochemical study of flotillin-1 in rat testis with ischemia/reperfusion injury. Cell Biology International, 31: 609–614. doi: 10.1016/j.cellbi.2006.11.035
- Issue published online: 2 JAN 2013
- Article first published online: 2 JAN 2013
- Received 25 September 2006; revised 22 November 2006; accepted 29 November 2006
- Cathepsin D;
- Sertoli cell;
- Testicular torsion
To investigate the involvement of flotillin-1 in acute experimental testicular torsion, we examined the expression and cellular localization of flotillin-1 and cathepsin D in the rat testis with ischemia/reperfusion (I/R) injury. Western blot analysis showed that the expression of flotillin-1 increased significantly 6 h after I/R and that the level remained elevated for 48 h. Immunohistochemically, flotillin-1 was constitutively localized in some Sertoli cells, peritubular myoid cells, and interstitial cells in the normal testis. After I/R injury, Sertoli cells in the damaged tubules were intensely immunostained for flotillin-1 at 24 and 48 h after I/R. Flotillin-1 was also detected in some inflammatory cells in the interstitial space around damaged tubules. Furthermore, flotillin-1 was colocalized with cathepsin D, a lysosomal marker, in normal testis (mainly in Sertoli cells), and the colocalization was greater in Sertoli cells and macrophages in I/R injured testes. Therefore, we postulate that flotillin-1 immunoreactivity is increased in some Sertoli and inflammatory cells (especially in ED1-positive activated macrophages) in testicular torsion and that flotillin-1 in the injured testis associates with lysosomes in Sertoli cells and macrophages, activating subsequent signals in inflammatory macrophages and Sertoli cells after I/R.