Role of connexin 43 in ischemic preconditioning does not involve intercellular communication through gap junctions

2004 ◽  
Vol 36 (1) ◽  
pp. 161-163 ◽  
Author(s):  
X Li
2017 ◽  
Vol 130 (21) ◽  
pp. 3619-3630 ◽  
Author(s):  
Teresa M. Ribeiro-Rodrigues ◽  
Tânia Martins-Marques ◽  
Sandrine Morel ◽  
Brenda R. Kwak ◽  
Henrique Girão

2015 ◽  
Vol 43 (3) ◽  
pp. 471-475 ◽  
Author(s):  
Teresa M. Ribeiro-Rodrigues ◽  
Steve Catarino ◽  
Maria J. Pinho ◽  
Paulo Pereira ◽  
Henrique Girao

Connexins (Cxs) are transmembrane proteins that form channels which allow direct intercellular communication (IC) between neighbouring cells via gap junctions. Mechanisms that modulate the amount of channels at the plasma membrane have emerged as important regulators of IC and their de-regulation has been associated with various diseases. Although Cx-mediated IC can be modulated by different mechanisms, ubiquitination has been described as one of the major post-translational modifications involved in Cx regulation and consequently IC. In this review, we focus on the role of ubiquitin and its effect on gap junction intercellular communication.


2011 ◽  
Vol 315A (6) ◽  
pp. 329-336 ◽  
Author(s):  
Katarzyna Marchlewska ◽  
Krzysztof Kula ◽  
Renata Walczak-Jedrzejowska ◽  
Elzbieta Oszukowska ◽  
Eliza Filipiak ◽  
...  

2015 ◽  
Vol 43 (3) ◽  
pp. 489-494 ◽  
Author(s):  
Sakthivel Vaiyapuri ◽  
Gagan D. Flora ◽  
Jonathan M. Gibbins

Platelets are involved in the maintenance of haemostasis but their inappropriate activation leads to thrombosis, a principal trigger for heart attack and ischaemic stroke. Although platelets circulate in isolation, upon activation they accumulate or aggregate together to form a thrombus, where they function in a co-ordinated manner to prevent loss of blood and control wound repair. Previous report (1) indicates that the stability and functions of a thrombus are maintained through sustained, contact-dependent signalling between platelets. Given the role of gap junctions in the co-ordination of tissue responses, it was hypothesized that gap junctions may be present within a thrombus and mediate intercellular communication between platelets. Therefore studies were performed to explore the presence and functions of connexins in platelets. In this brief review, the roles of hemichannels and gap junctions in the control of thrombosis and haemostasis and the future directions for this research will be discussed.


2007 ◽  
Vol 77 (Suppl_1) ◽  
pp. 205-205
Author(s):  
Mary Laws ◽  
Francesco DeMayo ◽  
John Lydon ◽  
Milan Bagchi ◽  
Indrani Bagchi

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Harissios Vliagoftis ◽  
Cory Ebeling ◽  
Ramses Ilarraza ◽  
Salahaddin Mahmudi-Azer ◽  
Melanie Abel ◽  
...  

Eosinophils circulate in the blood and are recruited in tissues during allergic inflammation. Gap junctions mediate direct communication between adjacent cells and may represent a new way of communication between immune cells distinct from communication through cytokines and chemokines. We characterized the expression of connexin (Cx)43 by eosinophils isolated from atopic individuals using RT-PCR, Western blotting, and confocal microscopy and studied the biological functions of gap junctions on eosinophils. The formation of functional gap junctions was evaluated measuring dye transfer using flow cytometry. The role of gap junctions on eosinophil transendothelial migration was studied using the inhibitor 18-a-glycyrrhetinic acid. Peripheral blood eosinophils express Cx43 mRNA and protein. Cx43 is localized not only in the cytoplasm but also on the plasma membrane. The membrane impermeable dye BCECF transferred from eosinophils to epithelial or endothelial cells following coculture in a dose and time dependent fashion. The gap junction inhibitors 18-a-glycyrrhetinic acid and octanol did not have a significant effect on dye transfer but reduced dye exit from eosinophils. The gap junction inhibitor 18-a-glycyrrhetinic acid inhibited eosinophil transendothelial migration in a dose dependent manner. Thus, eosinophils from atopic individuals express Cx43 constitutively and Cx43 may play an important role in eosinophil transendothelial migration and function in sites of inflammation.


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