title: [The effects of lipoproteins on human vascular endothelial gap junctional intercellular communication].
abstract: The effects of HDL, LDL and ascorbic acid on cultured human vascular endothelial gap junctional intercellular communication (GJIC) were observed using fluorescence recovery after photobleaching assay under confocal laser scanning microscopy in this study. The results showed that in culture, human vascular endothelial cells could produce functional gap junctions. The fluorescence recovery rates of the LDL group were 6.691 +/- 2.634, 4.153 +/- 2.125 and 2.441 +/- 0.720 respectively; when these rates were compared with the control and with each other, significant differences were found(P < 0.05). When the fluorescence recovery rates of the HDL group and Vitamin C group were compared with the control, no significant differences were found(P > 0.05). The fluorescence recovery rates of the LDL + HDL group were 3.500 +/- 0.890, 4.339 +/- 1.126 and 5.243 +/- 1.278(n = 15) respectively, when these rates were compared with the control and with each other, significant differences were found (P < 0.05). These suggested that LDL should be able to inhibit GJIC in human vascular endothelial cells, and the inhibition could be diminished by HDL or ascorbic acid. Inhibition of vascular endothelial GJIC may be one of the atherosclerogenic mechanisms of LDL, whereas HDL and ascorbic acid may be conducive to the improvement of endothelial GJIC. But it may also be only a compensatory behavior of endothelial cells to injuries.
authors.affiliation: Department of Cardiology, First Affiliated Hospital, WCUMS, Chengdu 610041.
authors.forename: Y
authors.initials: Y
authors.lastname: Liang
authors.forename: Z
authors.initials: Z
authors.lastname: Zeng
authors.forename: D
authors.initials: D
authors.lastname: Huang
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.forename: M
authors.initials: M
authors.lastname: Ren
authors.forename: O
authors.initials: O
authors.lastname: Qiang
mesh_terms: D001161:Arteriosclerosis / Q000209:etiology; D001205:Ascorbic Acid / Q000494:pharmacology; D002450:Cell Communication / Q000187:drug effects; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology*; D017629:Gap Junctions / Q000187:drug effects*; D006801:Humans; D008075:Lipoproteins, HDL / Q000494:pharmacology*; D008077:Lipoproteins, LDL / Q000494:pharmacology*; D018613:Microscopy, Confocal
chemical_list: D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D001205:Ascorbic Acid