Sulfated glycoprotein-2 induced endogenous resistance to ischemia and reperfusion injury in the seminiferous tubules.
Evidence of increased resistance of Sertoli cells to ischemia and reperfusion injury was presented by numerous histological, morphological, and quantitative studies. In situ hybridization techniques and immunocytochemical studies demonstrated intense expression of sulfated glycoprotein-2 (SGP-2) in Sertoli cells. We propose that protective effects of SGP-2 are the core of the differential tolerance of ischemia by the various testicular cells and the morphology of the postischemic testis. We believe that suppression of ischemic damage selectively in Sertoli cells is the consequence of the ability to produce SGP-2, an endogenous inhibitor of ischemic injury. This hypothetical function of SGP-2 is supported by its immunosuppressive properties and its structural and functional identity to several types of human complement cytolysis inhibitors.
Leibovitch
I
I
Department of Urology, Chaim Sheba Medical Center, Tel-Hashomer, Israel.
Buttyan
R
R
D000818:Animals; D051152:Clusterin; D006023:Glycoproteins / Q000502:physiology*; D006801:Humans; D007113:Immunity, Innate; D007511:Ischemia / Q000503:physiopathology*; D008297:Male; D008954:Models, Biological; D018832:Molecular Chaperones; D015427:Reperfusion Injury / Q000503:physiopathology*; D012671:Seminiferous Tubules / Q000098:blood supply*; D012708:Sertoli Cells / Q000502:physiology*
C495242:CLU protein, human; D051152:Clusterin; D006023:Glycoproteins; D018832:Molecular Chaperones