期刊
BRITISH JOURNAL OF PHARMACOLOGY
卷 147, 期 5, 页码 486-495出版社
WILEY
DOI: 10.1038/sj.bjp.0706631
关键词
gap junction; connexin; arrhythmia; cardiac myocytes; antiarrhythmic peptide; intercellular communication
1 We investigated the effects of rotigaptide (ZP123), a stable hexapeptide with antiarrhythmic properties, on gap junction mediated intercellular communication in contracting rat neonatal cardiac myocytes, HL-1 cells derived from cardiac atrium and in HeLa cells transfected with cDNA encoding Cx43-GFP, Cx32-GFP, Cx26-GFP, wild-type Cx43 or wild-type Cx26. 2 Intercellular communication was monitored before and after treatment with rotigaptide following microinjection of small fluorescent dyes (MW <1 kDa). The communication-modifying effect of rotigaptide was confined to cells expressing Cx43 since the peptide had no effect on dye transfer in HeLa cells expressing Cx32-GFP, Cx26-GFP or wild-type Cx26. In contrast, HeLa cells expressing Cx43-GFP exposed to 50 nM rotigaptide for 5 h showed a 40% increase in gap junction mediated communication. 3 Rotigaptide ( 50 nM) increased intercellular dye transfer in myocytes and atrial HL-1 cells, where Cx43 is the dominant connexin. However, it caused no change in cell beating rates of cardiac myocytes. 4 Western blot analysis showed that rotigaptide did not modify the overall level of Cx43 expression and changes in the phosphorylation status of the protein were not observed. 5 We conclude that the effects of rotigaptide were confined to cells expressing Cx43.
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