Background:

Cyclosporine (cyclosporin A), a immunosuppressive agent, inhibits phosphatase activity of calcineurin with IC50 value of 5 nM [1].
The immunosuppressive agent cyclosporin A (CsA) binds to soluble cytosolic proteins named cyclophilins, and the complex of cyclophilin–CsA blocks calcineurin, which inhibits stimulation of the NFAT-induced genes which are required for the activation of T cells.
As a widely used immunosuppressive agent, cyclosporin A has been reported to be effective against HCV infection. The anti-viral effects of CsA has been investigated by an HCV replicon system. Huh7/Rep-Feo cells treated with CsA with an IC50 value of about 0.5 μg/ml resulted in suppression of the replication of the HCV replicon in a dose-dependent manner. There were no changes in the rate of cell growth or viability, revealing that the specific effect of CsA against HCV is not due to cytotoxicity. CsA inhibits HCV replication in vitro specifically at clinical concentrations [2].
Transplantation of CSA-expanded FCV cells to chronic myocardial infarction was performed in the model of rat. Transplanted FCV cells were successfully differentiated into cardiomyocytes and integrated in the infarct heart to form GFP+/cTnT+ donor cell-derived cardiomyocyte bundle in the scar tissue in 2 weeks after the injection. The result show that CSA-expanded FCV cells can show highly cardiogenic potentials also in vivo after cell transplantation [3].
参考文献:
[1]. Fruman DA , Klee CB, Bierer BE, et al. Calcineurin Phosphatase-Activity In Lymphocytes-T Is Inhibited By Fk-506 And Cyclosporine-A. Proceedings Of The National Academy Of Sciences Of The United States Of America. 1992, 89(9): 3686-3690.
[2]. Nakagawa M, Sakamoto N, Enomoto N, et al. Specific inhibition of hepatitis C virus replication by cyclosporin A. Biochemical And Biophysical Research Communications. 2004, 313(1): 42-47.
[3]. Yan P, Nagasawa A, Uosaki H, et al. Cyclosporin-A potently induces highly cardiogenic progenitors from embryonic stem cells. Biochemical And Biophysical Research Communications. 2009, 379(1): 115-120.