Full Length Research Paper
Abstract
Gene therapy of detrusor underactivity, by autologous cells transplantation, is limited by the number of primary myogenic. The purpose of this study was to investigate whether Myod1 could induce primary bladder fibroblasts to undergo myogenic conversion. Primary bladder fibroblasts from Sprague-Daley rats were cultured. The eukaryotic expression plasmid pEGFP-Myod1 carrying both a rat Myod1 cDNA and a green fluorescent protein reporter gene was constructed and identified. The cultured primary bladder fibroblasts were transfected by pEGFP-Myod1 with Lipofection 2000 reagent. The results showed that expression of Myod1 could cause myogenic differentiation of bladder fibroblasts. These findings support the possibility of an alternative approach to exploit the capacity of Myod1 to activate myogenesis in bladder fibroblasts ex vivo and to create a vast source of autologous myogenic cells for gene therapy of detrusor underactivty by cell transplantation.
Key words: Fibroblasts, Myod1, gene therapy, detrusor underactivity.
Abbreviation
DU, Detrusor underactivity; RT, reverse transcriptase; PCR,polymerase chain reaction; MHC, myosin heavy chain; DMEM, Dulbecco’s modified Eagle’s minimal essential medium; FBS, fetal bovine serum; GFP, green fluorescent protein; BOO, bladder outlet obstruction; BPH, benign prostatic hyperplasia.
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