scholarly journals Connexin 43 mediated gap junctional communication enhances breast tumor cell diapedesis in culture

2005 ◽  
Vol 7 (4) ◽  
Author(s):  
Mary-Ann Pollmann ◽  
Qing Shao ◽  
Dale W Laird ◽  
Martin Sandig
1995 ◽  
Vol 16 (7) ◽  
pp. 1505-1511 ◽  
Author(s):  
Charles S. T. Hii ◽  
Antonio Ferrante ◽  
Simon Schmidt ◽  
Deborah A. Rathjen ◽  
Brenton S. Robinson ◽  
...  

1994 ◽  
Vol 19 (3) ◽  
pp. 173-177 ◽  
Author(s):  
Hideki Chiba ◽  
Norimasa Sawada ◽  
Masahito Oyamada ◽  
Takashi Kojima ◽  
Kousuke Iba ◽  
...  

Neuroreport ◽  
2017 ◽  
Vol 28 (4) ◽  
pp. 208-213 ◽  
Author(s):  
Lilia Y. Kucheryavykh ◽  
Jan Benedikt ◽  
Luis A. Cubano ◽  
Serguei N. Skatchkov ◽  
Feliksas F. Bukauskas ◽  
...  

2017 ◽  
Vol 313 (4) ◽  
pp. C362-C370 ◽  
Author(s):  
Guangming Yang ◽  
Xiaoyong Peng ◽  
Yue Wu ◽  
Tao Li ◽  
Liangming Liu

We examined the roles played by gap junctions (GJs) and the GJ channel protein connexin 43 (Cx43) in arginine vasopressin (AVP)-induced vasoconstriction after hemorrhagic shock and their relationship to Rho kinase (ROCK) and protein kinase C (PKC). The results showed that AVP induced an endothelium-independent contraction in rat superior mesenteric arteries (SMAs). Blocking the GJs significantly decreased the contractile response of SMAs and vascular smooth muscle cells (VSMCs) to AVP after shock and hypoxia. The selective Cx43-mimetic peptide inhibited the vascular contractile effect of AVP after shock and hypoxia. AVP restored hypoxia-induced decrease of Cx43 phosphorylation at Ser262 and gap junctional communication in VSMCs. Activation of RhoA with U-46619 increased the contractile effect of AVP. This effect was antagonized by the ROCK inhibitor Y27632 and the Cx43-mimetic peptide. In contrast, neither an agonist nor an inhibitor of PKC had significant effects on AVP-induced contraction after hemorrhagic shock. In addition, silencing of Cx43 with siRNA blocked the AVP-induced increase of ROCK activity in hypoxic VSMCs. In conclusion, AVP-mediated vascular contractile effects are endothelium and myoendothelial gap junction independent. Gap junctions between VSMCs, gap junctional communication, and Cx43 phosphorylation at Ser262 play important roles in the vascular effects of AVP. RhoA/ROCK, but not PKC, is involved in this process.


1990 ◽  
Vol 3 (6) ◽  
pp. 335-343 ◽  
Author(s):  
Michael Rogers ◽  
John M. Berestecky ◽  
Mohammad Z. Hossain ◽  
Huiming Guo ◽  
Ranjana Kadle ◽  
...  

Zygote ◽  
2007 ◽  
Vol 15 (2) ◽  
pp. 149-157 ◽  
Author(s):  
M.E. Mónaco ◽  
E.I. Villecco ◽  
S.S. Sánchez

SummaryThe aim of the present study was to investigate the physiological role and the expression pattern of heterologous gap junctions during Xenopus laevis vitellogenesis. Dye transfer experiments showed that there are functional gap junctions at the oocyte/follicle cell interface during the vitellogenic process and that octanol uncouples this intercellular communication. The incubation of vitellogenic oocytes in the presence of biotinylated bovine serum albumin (b-BSA) or fluorescein dextran (FDX), showed that oocytes develop stratum of newly formed yolk platelets. In octanol-treated follicles no sign of nascent yolk sphere formation was observed. Thus, experiments in which gap junctions were downregulated with octanol showed that coupled gap junctions are required for endocytic activity. RT-PCR analysis showed that the expression of connexin 43 (Cx43) was first evident at stage II of oogenesis and increased during the subsequent vitellogenic stages (III, IV and V), which would indicate that this Cx is related to the process that regulates yolk uptake. No expression changes were detected for Cx31 and Cx38 during vitellogenesis. Based on our results, we propose that direct gap junctional communication is a requirement for endocytic activity, as without the appropriate signal from surrounding epithelial cells X. laevis oocytes were unable to endocytose VTG.


Endocrinology ◽  
2005 ◽  
Vol 146 (9) ◽  
pp. 4054-4060 ◽  
Author(s):  
Nurul Kabir ◽  
Kirti Chaturvedi ◽  
Lian Sheng Liu ◽  
Dipak K. Sarkar

Abstract Folliculostellate (FS) cells are known to communicate with each other and with endocrine cells via gap junctions in the anterior pituitary. We investigated whether TGFβ3 and estradiol, known to regulate FS cell production and secretion of basic fibroblast growth factor (bFGF), increases gap junctional communication to alter bFGF secretion from FS cells. FS cells in monolayer cultures were treated with TGFβ3 or vehicle alone for 24 h and then microinjected with Lucifer Yellow and high-molecular-weight Texas Red dextran. Ten minutes later the transfer of dye among adjacent cells was recorded with a digital microscope. TGFβ3 increased the transfer of dye. The TGFβ3-neutralizing antibody and the gap junction inhibitor octanol reduced the effect of TGFβ3 on the transfer of dye. The TGFβ3-induced transfer of dye was unaltered by simultaneous treatment with estradiol. The steroid alone also had no effect. TGFβ3 increased total and phosphorylated levels of connexin 43. Estradiol treatment did not produce any significant changes on basal or TGFβ3-induced increases in connexin 43 levels. The gap-junction inhibitor octanol reduced TGFβ3-increased levels of bFGF in FS cells. Taken together, these results suggest that TGFβ3 may act on FS cells to increase gap-junctional communication to maximize its effect on bFGF secretion.


2006 ◽  
Vol 2 (1) ◽  
pp. 3-14 ◽  
Author(s):  
VANESSA HOUADES ◽  
NATHALIE ROUACH ◽  
PASCAL EZAN ◽  
FRANK KIRCHHOFF ◽  
ANNETTE KOULAKOFF ◽  
...  

The high level of intercellular communication mediated by gap junctions between astrocytes indicates that, besides individual astrocytic domains, a second level of organization might exist for these glial cells as they form communicating networks. Therefore, the contribution of astrocytes to brain function should also be considered to result from coordinated groups of cells. To evaluate the shape and extent of these networks we have studied the expression of connexin 43, a major gap junction protein in astrocytes, and the intercellular diffusion of gap junction tracers in two structures of the developing brain, the hippocampus and the cerebral cortex. We report that the shape of astrocytic networks depends on their location within neuronal compartments in a defined brain structure. Interestingly, not all astrocytes are coupled, which indicates that connections within these networks are restricted. As gap junctional communication in astrocytes is reported to contribute to several glial functions, differences in the shape of astrocytic networks might have consequences on neuronal activity and survival.


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