[Effects of paclitaxel combined with bone marrow stromal stem cells implantation on vascular endothelial repair and smooth muscle cells growth in vitro].

OBJECTIVE: To investigate the effects of paclitaxel combined with bone marrow stromal stem cells (MSCs) implantation on inhibiting the smooth muscle cells (SMCs) growth and promoting endothelial repair by developing an endothelial repair model in vitro. METHODS: In a cell coculture system, rabbit endothelial cells (ECs) and human MSCs were seeded in the lower chamber and rabbit SMCs were seeded in the upper chamber. 3H-TdR incorporation and PCNA protein expression were used to evaluate SMCs proliferation at the 10th day after paclitaxel application (1, 10, 100 nmol/L; 20 min). Fluorescence immunocytochemistry was employed to observe the Flk-1 and vWF protein expression on MSCs. RESULTS: The SMCs 3H-TdR incorporation of the MSCs implant group was significantly lower than that of the proliferative ECs group (1 nmol/L: 12 265 +/- 991 vs. 14 505 +/- 1013 cpm/well; 10 nmol/L: 8401 +/- 783 vs. 10 511 +/- 934 cpm/well; 100 nmol/L: 5880 +/- 569 vs. 7457 +/- 768 cpm/well, n = 6, P < 0.05), but higher than that of the confluent ECs group (1 nmol/L: 12 265 +/- 991 vs. 8671 +/- 642 cpm/well; 10 nmol/L: 8401 +/- 783 vs. 6175 +/- 743 cpm/well; 100 nmol/L: 5880 +/- 569 vs. 4423 +/- 406 cpm/well, n = 6, P < 0.05). The expression of SMCs PCNA protein in MSCs implant group was lower than that of the proliferative ECs group (1 nmol/L: 0.92 +/- 0.06 vs. 1.15 +/- 0.07; 10 nmol/L: 0.97 +/- 0.07 vs. 1.07 +/- 0.08; 100 nmol/L: 0.91 +/- 0.05 vs. 1.18 +/- 0.11, n = 6, P < 0.05), but higher than that of the confluent ECs group (1 nmol/L: 0.92 +/- 0.06 vs. 0.74 +/- 0.07; 10 nmol/L: 0.97 +/- 0.07 vs. 0.78 +/- 0.06; 100 nmol/L: 0.91 +/- 0.05 vs. 0.71 +/- 0.05, n = 6, P < 0.05). The MSCs did not express vWF or Flk-1 protein before coculture. Although none cell expressed vWF, some of the MSCs began to express Flk-1 protein after cocultured with mature ECs for 10 days. CONCLUSION: MSCs implantation can partly inhibit the delayed SMCs proliferation. The MSCs cocultured with paclitaxel-treated mature ECs have the ability to differentiate into ECs.