兔髂动脉内膜损伤后PDGF-BmRNA在血管壁原位表达增强

目的:探讨内膜损伤后血管平滑肌细胞(VSMCS)增殖的体内机制。方法:用球囊导管损伤兔髂动脉内膜建立VSMCS增殖模型,以自行设计、合成的血小板源性生长因子β(PDGF-B)cDNA探针和原位杂交方法检测了损伤后不同时期VSMCS表达PDGF-B mRNA与VSMCS表达增殖细胞核抗原和内膜横断面积增加关系。 结果:血管损伤后VSMCS 表达PDGF-B mRNA增强,计数内膜(0.25 mm×mm)×4面积中PDGF-B mRNA阳性细胞数分别为1、2和4周的31.93±14.63,26.50±9.25和24.85±13.65。其表达与VSMCS表达增殖细胞核抗原和内膜面积的增加密切相关。结论: 血管内膜损伤后VSMCS自泌性产生PDGF-B 是VSMCS增殖和内膜增生的主要原因之一。我们设计的探针为原位研究兔VSMCS PDGF-B mRNA的表达提供方便。

The in situ expression of PDGF-B mRNA increased after the denudation of rabbit iliac arteries

AIM: To elucidate the in vivo mechanisms of the proliferation of vascular smooth muscle cells (VSMCS) in injuried arteries. METHODS: A VSMCS proliferative model was constructed by injury of rabbit iliac arteries with balloon catheters and a probe designed for rabbit platelet-derived growth factor B chain (PDGF-B ) mRNA was used to detect the expression of it by intimal VSMCS on the vascular cross sections using an in situ hybridization technique at the indicated times. The relation of this expression to the proliferation of VSMCS by their expression of proliferating cell nuclear antigen (PCNA) and vascular intimal areas were estimated. RESULTS: The expression of PDGF-B mRNA of intimal VSMCS was increased when calculating the intimal PDGF-B mRNA positive cells per millimetre area at ×400 magnification with average numbers of 31.93±14.64 in 1 week group, 26.50±9.25 in 2 weeks group and 24.85±13.65 in 4 weeks group. This was in accordance with the expression of PCNA by VSMCS and the increase of intimal areas. CONCLUSION: The local production of PDGF-B by VSMCS via an autocrine mechanism is responsible for the continuous proliferation of these cells and formation of neointima after the injury. The probe designed is very useful for detecting rabbit PDGF-B mRNA.