Objec

tive      To observe the epithelial-mesenchymal transition (EMT) of human intrahepatic biliary epithelial cells (HIBECs) induced by cold preservation reperfusion injury (CPRI)

and to study the role of tricho-rhino-pharyngeal syndrome type 1 (Trps1) in the occurrence of HIBECs EMT.       Methods      HIBECs were incubated with simulated CPR1 in vitro

then expressions of E-cadherin

CK19

Vimentin

α-SMA and the target gene Trps1 in HIBECs were detected by RT-PCR and Western blotting after treatment of HIBECs with CPRI.  The effect of Trps1 was increased with recombinant adenovirus vector containing Trps1 gene or blocked with Trps1 siRNA

then the role of Trps1 was studied.       Results      With the prolongation of cold preservation time

the mRNA and protein expression of EMT markers

E-cadherin and CK19 was decreased (

P

=0.018

0.011;

P

=0.039

0.044)

while that of Vimentin and α-SMA was significantly increased (

P

=0.002

0.026;

P

=0.035

0.016). The expression of Trps1 mRNA and protein reached its peak at 12 h (

P

=0.018

0.031) and began to decrease at 24 and 48 h

respectively (

P

=0.026

0.009). Trps1 was positively correlated with the epithelial markers (r=0.981

0.913;

P

=0.000

0.002) but negatively correlated with the mesenchymal markers (r=-0.711

-0.847;

P

=0.009

0.005). Recombinant adenovirus vector containing Trps1 gene could up-regulate the CPRI-induced expression decrease of E-cadherin (

P

=0.002

0.000) but down-regulate the expression increase of Vimentin (

P

=0.000

0.017). Trps1 siRNA could down-regulate the CPRI-induced expression decrease of E-cadherin (

P

=0.032

0.044) but up-regulate the expression increase of Vimentin and α-SMA (

P

=0.047

0.031).       Conclusion      CPRI can induce the occurrence of HIBECs EMT. Trps1 participates in the regulation of HIBECs EMT as a key antagonistic factor

and may reverse the process.