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Abrogation of chronic rejection in rat model system involves modulation of the mTORC1 and mTORC2 pathways.
|Title||Abrogation of chronic rejection in rat model system involves modulation of the mTORC1 and mTORC2 pathways.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Zhang L, You J, Sidhu J, Tejpal N, Ganachari M, Skelton ST, Kloc M, Li XC, Ghobrial RM|
|Date Published||2013 Nov 15|
Current immunosuppressive regimens fail to avert chronic rejection (CR) of transplanted organs; however, selective targeting of actin-cytoskeletal regulators decreases T-cell motility and abrogates CR in rat model system. Administration of mutated class I major histocompatibility complex molecules or selective targeting of the RhoA pathway, which controls T-cell cytoskeletal activity, using Y27632 (a selective Rock1 inhibitor) resulted in reduced T-cell infiltration and abrogation of CR as judged from the neointimal index (13.9±19.7 vs. 45±37.5; P<0.001) and the number of affected vessels (30% vs. 60%; P<0.01). Here, we examined the role of mammalian target of rapamycin (mTOR) pathway in inhibition of CR.