Event Title
Differential Expression of Cyclophilin A in Cyclosporine A induced Renal Fibrosis
Location
Suwanee, GA
Start Date
14-5-2019 1:00 PM
End Date
14-5-2019 4:00 PM
Description
Kidney fibrosis, the hallmark of chronic kidney diseases, has the features of extracellular matrix accumulation, tubular atrophy, inflammatory cell infiltration and peritubular microvasculature loss. It has been suggested that multiple cell components including epithelial, fibroblasts, endothelial and inflammatory cells all contribute to fibrosis progression. Cyclosporine A (CsA) is an immunosuppressive drug used to prevent organ rejection, in transplant patients. CsA has several side effects which include: viral infection, chronic renal insufficiency, end-stage renal disease, cancer and new-onset diabetes. We are focused on its nephrotoxicity properties. CsA immunosuppressive properties are accomplished by inhibiting the activation of T-cells. The objective of the study is to examine Cyclophilin A (CyPA) levels, when treated with CsA, in kidney epithelial and fibroblast cells. CyPA forms a binding complex with CsA. This complex inhibits Calcineurin (CnA) bind to CsA. To evaluate CyPA levels, cells are treated with 100ng of CsA, in a six well plate, for 24 and 48 hours. The protein lysates are collected using TNESV lysis buffer and a Western Blot was used to observe CyPA expression. Our current results show that kidney epithelial and fibroblast cells express different levels of MMP-9, MMP-2, TGF-b, CnA-band CnA-a when treated with CsA versa when not treated with CsA. CyPA is a known CsA binding protein. We expect CyPA levels to increase when cells are treated with CsA. We see significant decrease in CyPA after 24 and 48 hours. In conclusion, our data suggest that CyPA deceases significantly in the presents of CsA, due to a binding complex formation.
Embargo Period
1-28-2020
Differential Expression of Cyclophilin A in Cyclosporine A induced Renal Fibrosis
Suwanee, GA
Kidney fibrosis, the hallmark of chronic kidney diseases, has the features of extracellular matrix accumulation, tubular atrophy, inflammatory cell infiltration and peritubular microvasculature loss. It has been suggested that multiple cell components including epithelial, fibroblasts, endothelial and inflammatory cells all contribute to fibrosis progression. Cyclosporine A (CsA) is an immunosuppressive drug used to prevent organ rejection, in transplant patients. CsA has several side effects which include: viral infection, chronic renal insufficiency, end-stage renal disease, cancer and new-onset diabetes. We are focused on its nephrotoxicity properties. CsA immunosuppressive properties are accomplished by inhibiting the activation of T-cells. The objective of the study is to examine Cyclophilin A (CyPA) levels, when treated with CsA, in kidney epithelial and fibroblast cells. CyPA forms a binding complex with CsA. This complex inhibits Calcineurin (CnA) bind to CsA. To evaluate CyPA levels, cells are treated with 100ng of CsA, in a six well plate, for 24 and 48 hours. The protein lysates are collected using TNESV lysis buffer and a Western Blot was used to observe CyPA expression. Our current results show that kidney epithelial and fibroblast cells express different levels of MMP-9, MMP-2, TGF-b, CnA-band CnA-a when treated with CsA versa when not treated with CsA. CyPA is a known CsA binding protein. We expect CyPA levels to increase when cells are treated with CsA. We see significant decrease in CyPA after 24 and 48 hours. In conclusion, our data suggest that CyPA deceases significantly in the presents of CsA, due to a binding complex formation.