期刊
LIFE SCIENCES
卷 122, 期 -, 页码 72-77出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2014.12.009
关键词
Dexmedetomidine; Gap junction intercellular communication; Hypoxia/reoxygenation; NRK-52E cell; Apoptosis; HeLa cell
资金
- National Natural Science Foundation of China [81170449]
- Natural Science Foundation of Guangdong Province, China [S2011020002780]
- Science and Technology Planning Project of Guangdong Province, China [2012B061700071]
Aims: The alpha 2-adrenoceptor inducer dexmedetomidine (Dex) provides renoprotection against ischemia/reperfusion (I/R) injury, but the mechanism of this effect is largely unknown. The present study investigated the effect of Dex on apoptosis induced by hypoxia/reoxygenation (H/R) and the relationship between this effect and gap junction intercellular communication (GJIC). Main methods: In vitro, two cell lines of normal rat kidney proximal tubular cells (NRK-52E) and HeLa cells that were transfected with a connexin 32 (Cx32) plasmid were exposed to H/R. The role of Dex in the modulation of H/R-induced apoptosis was explored by the manipulation of connexin expression, and hence gap junction (GJ) function, using a GJIC inhibitor, heptanol, and a GJIC inducer, retinoic acid. GJ function and the Cx32 protein level were determined by the parachute dye-coupling assay and Western blotting, respectively. Key findings: Dex and heptanol significantly reduced H/R-induced apoptosis in NRK-52E cells. The anti-apoptosis effect of Dex was exhibited only in Cx32-expressing HeLa cells. One hour Dex exposure inhibited GJ function mainly via a decrease in Cx32 protein levels in NRK-52E cells. Significance: Our data suggest that Dex reduced H/R-induced apoptosis through the inhibition of GJ activity by reducing Cx32 protein levels. (C) 2014 Elsevier Inc. All rights reserved.
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