The Effect Of Oxidized Low Density Lipoprotein On Expression Of Cxcr4 In Mouse Bone Marrow-derived Smooth Muscle Progenitor Cell.

Background The chemokine stromal cell derived-factor1(SDF-1)also name CXCL12 or pro-B stimulating factor and belong to the intercrine CXC subfamily. The single SDF-1 gene encode two kinds protein:SDF-1αand SDF-1β.SDF-1 major express on hematopoietic stem cells.CXCR4 is the single chemokine receptor of SDF-1, which is a seven-transmembrane domain, GTP-binding protein-coupled receptor and is high expression in hematopoietic stem/progenitor cells and endothelial progenitor cells. Newly investigation indicate that CXCR4 also express on marrow stromal cells(MSC).Literature report that the myocardium after myocardial infarction(MI) will immediately up-regulate the SDF-1 and induce over-expression of CXCR4 to migration in ischemic myocardium. In the Zhang's investigation manifest the CXR4+ MSC has participated in the form of the new vessels and differentiate to original myocardical cells; animal studies indicate the interaction of SDF-1/CXCR4 axis play a critical role in the repair myocardium through recruitment MSC. Study with the mouse which are knocked-out of SDF-1 and/or CXCR4 has indicate the SDF-1/CXCR4 axis also play a important role in the cell differentiation. MSC is a crucial cell component in the bone marrow microenvironment, which has potency to differentiate to various kinds of cells, and a literature report that MSC can differentiate into the smooth muscle progenitor cells(SPC).The bone marrow-derived MSC or SPC is the significant source of smooth muscle cell in the plaque of the atherosclerosis(As).Then ,we are still unknown that during the plaque to form and reparation of the As whether the SDF-1/CXCR4 recruitment MSC or SPC homing to damage arteries and take part in the shape of As or not. Object Oxidized Low Density Lipoprotein (ox-ldl) is a risk factor of As. Now to detect the effect of ox-ldl on CXCR4, which is the receptor of SDF-1, expression in mouse bone marrow-derived SPC .To explore the contribution of SDF-1/CXCR4 to homing SPC to arterial damage.Methods SPC was incubated with the same concentration (50μg/mL), CXCR4 mRNA and protein was revealed by RT-PCR, Western-Blot ,immunofluorescence staining and confocal laser scanning microscope analysis respectively. To observe the time-effect relationship between ox-ldl and the SPC expression of CXCR4.Results Ox-ldl did not give to the SPC but it has the foundational level of CXCR4 expression,50μg/mL of ox-ldl stimulate SPC 0-72h,during the stimulation time ,CXCR4 expression gradually,36h reached peak, and its mRNA and protein levels were 5.73 folds and 5.02 folds of the basis level ,the differences were statistically significant(p<0.05),then decreased gradually, but still higher than the basis level. Immunofluorescence staining and confocal laser scanning microscope analysis detection in 0h observed when ox-ldl did not give SPC stimulated the cytoplasm and cell membrane surface of a small number of CXCR4 expression, with the extension of time ,CXCR4 expression gradually increases the volume when in 36h in the SPC and the cycoplasmic membrane surface expression of the strongest,60h the expression of CXCR4 decreased gradually.Conclusions Ox-ldl can increase in mouse bone marrow-derived SPC CXCR4 expression ,suggesting the possibility of ox-ldl by upregulate the expression of SPC CXCR4 to induced migration and homing of SPC to the artery lesions to participate in the formation of As.