培养的内皮细胞和平滑肌细胞之间间隙连接形成及连接通讯的研究

本实验以离子电渗法将荧光黄注入细胞内,观察培养的EC 与SMC 同类及异类细胞间连接通讯现象,证实SMC 与EC 在培养中可形成同类或异类细胞GJ 结构,两种细胞间有接触介导的物质交流。EC-EC 之间的细胞通讯比SMC-SMC 和SMC-EC 之间为强。对SMC 有促增殖作用的LDL(100 μg LDL-蛋白质/ml)及胰岛素(15 mu/ml)对这种连接通讯有抑制作用,促癌剂TPA 几乎完全抑制此种连接通讯。结果提示高浓度LDL 及胰岛素等可能通过抑制SMC 与EC 之间的连接通讯而使SMC 脱离正常控制而大量增殖,促进AS发生、发展。故推论促进细胞连接通讯的因子,可能对AS 有防治作用,值得进一步研究。

STUDIES ON GAP JUNCTION FORMATION AND JUNCTIONAL COMMUNICATION BETWEEN CULTURED ENDOTHELIAL CELLS AND SMOOTH MUSCLE CELLS

Gap junction(GJ)between two con-tacted cells is the structural basis of in-tercellular communication.Gap junctiontransfer plays an important role in regu-lation of cell proliferation.Culturedendothelial cells(EC)and smoothmuscle cells(SMC)were injected withfluorescein Lucifer Yellow by iontophoreticinjection,and examined under fluoresceinmicroscope,We have demonstrated thatthere existed homologous and heterologousGJ and contact mediated dye transfer be-tween cultured EC and SMC.LDL and in-sulin which promote SMC proliferationmay inhibit the junctional communicationbetween SMC and EC.Tumor promoterTPA induced almost complete inhibitionof junctional communication between ECand SMC.The results indicate that normally re-gulative signals of metabolism and growthare transfered between EC and SMC viajunctional communication to maintain thevessel wall homeostasis,Highdosage LDLand insulin may keep SMC away fromnormal growth control and induce theirproliferation by means of inhibitingjunctional communication.It may be oneof important mechanisms of athero-genesis.