Role of protocadherin 20 in spinal cord in development of bone cancer pain in rats / 中华麻醉学杂志

ABSTRACT

Objective To investigate the effects of protocadherin 20 (PCDH20) in the spinal cord in the development of bone cancer pain (BCP) in rats.Methods Thirty-six SPF female Sprague-Dawley rats,weighing 180-200 g,were randomly divided into 4 groups (n =9 each)sham operation group (group S),BCP group,lentivirus control group (group LC) and PCDH20 siRNA lentivirus group (group P).Control lentivirus and lentivirus containing PCDH20 siRNA 4 μl were injected into the ipsilateral spinal cord in groups LC and P,respectively.One week later,BCP was induced by injection of Walker 256 breast cancer cells into the upper segment of bone marrow of right tibia.The mechanical paw withdrawal threshold (MWT) was measured at 1 day before injection of lentivirus (T1),1 day before BCP (T2),and 7,14 and 21 days after BCP (T3-5).Three rats in each group were sacrificed after measurement of the MWT at 21 day after BCP and the tibia on the operated side was obtained for examination of invasion of the cancer cells with light microscope.The spinal cord was removed for determination of the expression of PCDH20 and postsynaptic density 95 (PSD95) protein (by Western blot) and mRNA (by RTPCR).Results In groups BCP,LC and P,the cancer cells grew out of the bone and destroyed the cortical bone seriously.Compared with group S,the MWT was significantly decreased at T3-5 in groups BCP,LC and P,the expression of PCDH20 and PSD95 protein and mRNA was up-regulated in groups BCP and LC,and the expression of PCDH20 was up-regulated in group P (P ＜ 0.05).Compared with BCP group,no significant change was found in the MWT and expression of PCDH20 and PSD95 protein and mRNA in group LC (P ＞ 0.05),and the MWT was significantly increased at T4,5 and the expression of PCDH20 and PSD95 protein and mRNA was down-regulated in group P (P ＜ 0.05).Conclusion PCDH20 is involved in the development of BCP through regulating the expression of PSD95 in the spinal cord and adjusting the function of excitatory synapse in rats.