Cell cycle dependent regulation of gap junction coupling and apoptosis in GFSHR-17 granulosa cells英文文献资料.docVIP

J. Biomedical Science and Engineering, 2010, 3, 884-891 JBiSE doi:10.4236/jbise.2010.39118 Published Online September 2010 (http://www.SciRP.org/journal/jbise/). Cell cycle dependent regulation of gap junction coupling and apoptosis in GFSHR-17 granulosa cells Sabrina Schlie , Karolina Mazur , Willem Bintig , Anaclet Ngezahayo 1,2 1 1 1 1 2 Institute of Biophysics, University Hannover, Herrenh?userstr, Hannover, Germany; Laser Zentrum Hannover e.V., Hollerithallee, Hannover, Germany. Email: ngezahayo@biophysik.uni-hannover.de Received 26 November 2009; revised 10 March 2010; accepted 12 March 2010. ABSTRACT to-cell channels that enable neighbouring cells to excha- nge small molecules (≤ 1 kDa) like Ca , cAMP, IP3, and 2+ Recent results have shown that the level of gap junc- tion coupling could modulate the induction of apopt- otic reactions. We previously observed that 1H-[1,2, 4]Oxadiazole[4,3-a]quinoxalin-1-one (ODQ), a block- er of guanylyl cyclase, inhibited gap junction coup- ling and thereby promoted activation of characteris- tic apoptotic reactions such as chromatin condensa- tion, DNA strand breaking, and formation of blebs in GFSHR-17 granulosa cells, the in vitro model for gra- nulosa cells of the maturing ovular follicle. In the pr- esent report, we focus on the effects of ODQ with re- spect to the cell cycle in GFSHR-17 granulosa cells. In synchronised GFSHR-17 granulosa cells, the doub- le whole-cell patch-clamp technique revealed that gap junction conductance in mitotic cells was reduced in comparison to cells in interphase. This reduction of gap junction conductance correlated with a reduction of non-phosphorylated Cx43 in mitotic cells. We com- pared the stimulation of apoptotic reactions by ODQ between cells in mitosis and in interphase. We ob- served that the