Human THBD Stable Cell Line - CHO-K1

The trio of thrombocytopenia, renal failure, and microangiopathic hemolytic anemia makes up the hemolytic-uremic syndrome. The function of the endothelium glycoprotein thrombomodulin (THBD) in the atypical hemolytic-uremic syndrome (aHUS) was examined by the researchers. Among 152 aHUS patients, they found six heterozygous missense mutations in THBD. By fast-tracking factor I's inactivation of C3b, thrombomodulin binds to both C3b and factor H (CFH), controlling complement activation in vitro through the use of pure proteins and cell-expression systems. In cultured cells, thrombomodulin variants linked to aHUS showed reduced ability to inactivate C3b and activate procarboxypeptidase B, lowering defense against activated complement. These results emphasize the function of thrombomodulin in the pathophysiology of aHUS and its potential as a target for treatment.

Figure 1. CHO-K1 cells were transfected stably either with an empty vector (control) or with a vector expressing thrombomodulin. The CHO-K1 human THBD stable cell line was evaluated by the researchers for its ability to improve complement inactivation. Techniques included immunoblotting to detect CFH and C3b interaction with thrombomodulin and flow cytometry to quantify iC3b deposition. (Delvaeye M, et al., 2009)