Objective      To investigate the regulatory mechanisms of the plasticity of interstitial cells of Cajal (ICC) in the colon of adult mice with imatinib (STI571)-mediated Kit signaling blockage.       Methods      Forty-five 4-week-old healthy BALB/c mice (18 to 20 g) were divided into 5 groups including a control group (treated with identical doses of normal saline)

an 8 d group and a 16 d group after imatinib treatment

and an 8 d group and a 16 d group afte

r imatinib withdrawal. The number and shape changes of Kit

+

and CD44

+

ICC subtypes (ICC-MY

ICC-SM

ICC-IM

and ICC-SS) were revealed by fluorescence immunoassay with anti-Kit antibody and CD44 antibody. The protein and mRNA changes of Kit and CD44 were measured by Western blotting and real time RT-PCR

respectively.       Results      (1) Imatinib treatment led to a gradual reduction of Kit

+

ICC-IM and ICC-MY numbers to almost 50% that of the control group in day 16 (ICC-MY: 136.17±3.56 vs 66.74±1.47

P

0.05)

and the numbers recovered to normal within 16 d after imatinib withdrawal. (2) The number and network of Kit

+

ICC-SM did not change during the whole process. (3) Kit protein and mRNA also decreased in a time-dependent manner and recovered to normal after imatinib withdrawal. (4) The CD44

+

ICC did not change significantly in amount during the process

and neither did CD44 protein and mRNA.       Conclusion      Kit signaling regulates ICC plasticity in the colon of adult mice. ICC loses Kit phenotype after blockage of Kit signal pathway

while CD44 expression is not affected.