Aim To explore phenotypic modulation of vascular smooth muscle cells(VSMC) and change of p38,mitogen-activated protein kinase phosphatase-1(MKP-1) expression after intimal injury. Methods The model of vascular restenosis established by intimal injury of rabbit carotid arteries was used.Immunohistochemistry,Western blot and reverse transcriptase-polymerase chain reaction(RT-PCR) were used to detect the changes of proliferation cell nuclear antigen(PCNA),smooth muscle α-actin(SM α-actin),p38 protein,and MKP-1 protein as well as its mRNA of sham-injured arteries and injured arteries at different time points. Results PCNA was negative in the medium and endothelium in shaminjured arteries.Positive cell rate of PCNA was gradually increased at 1～14 days in the medium and at 5～14 days in the neointima after injury,but it declined gradually after 28 days.Positive cell rate of PCNA in the neointima was slightly more than that in the medium at different time points.SM α-actin was positive in the medium,negative in the endothelium in sham-injured arteries.SM α-actin initially decreased in the medium at 1 day,it was minimal at 3 days after injury,but it increased gradually after 5 days.Positive expression of SM α-actin in the neointima was slightly lower than that in the medium.p38 was negative or feeble positive in the medium in sham-injured arteries.p38 was continuously increased at 1～35 days after injury.Positive expression of p38 in the neointima was higher than that in the medium.There was positive relationship between change of p38 and that of PCNA in the vascular wall at different time points after injury.MKP-1 was feeble positive or positive in sham-injured arteries.MKP-1 initially decreased at 1 day and increased graduallv from 14～28th day,but it was still lower than that in the sham-injured arteries on 35th day after injury.There was negative relationship between change of MKP-1 and that of PCNA in the vascular wall at different time points after injury. Conclusion There was close relationship between phenotypic modulation and proliferation ability of VSMC.p38 and MKP-1 participated in phenotypic modulation of VSMC and its regulation after intimal injury.