ArticleCirculation research2005
Adenovirus vector E4 gene regulates connexin 40 and 43 expression in endothelial cells via PKA and PI3K signal pathways.
Article in Circulation research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Viral Infection and Connexin Dysfunction in the Heart.Current cardiology reports · 2025Review
- Adenovirus targets transcriptional and posttranslational mechanisms to limit gap junction function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Gap Junctions in the Bone Marrow Lympho-Hematopoietic Stem Cell Niche, Leukemia Progression, and Chemoresistance.International journal of molecular sciences · 2020Review
- Gap junction modulation and its implications for heart function.Frontiers in physiology · 2014Review
- CXCR4 gene transfer prevents pressure overload induced heart failure.Journal of molecular and cellular cardiology · 2012Article
- Inhibition of gap junctional Intercellular communication in WB-F344 rat liver epithelial cells by triphenyltin chloride through MAPK and PI3-kinase pathways.Journal of occupational medicine and toxicology (London, England) · 2010Article
- Endothelial cells are essential for the self-renewal and repopulation of Notch-dependent hematopoietic stem cells.Cell stem cell · 2010Article
- Prostaglandin promotion of osteocyte gap junction function through transcriptional regulation of connexin 43 by glycogen synthase kinase 3/beta-catenin signaling.Molecular and cellular biology · 2010Article
- Recombinant adenoviral vectors can induce expression of p73 via the E4-orf6/7 protein.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Connexins (Cxs) provide a means for intercellular communication and play important roles in the pathophysiology of vascular cardiac diseases. Infection of endothelial cells (ECs) with first-generation E1/E3-deleted E4+ adenovirus (AdE4+) selectively modulates the survival and angiogenic potential of ECs by as of yet unrecognized mechanisms. We show here that AdE4+ vectors potentiate Cx expression in ECs in vitro and in mouse heart tissue. Infection of ECs with AdE4+, but not AdE4-, resulted in a time- and dose-dependent induction of junctional Cx40 expression and suppression of Cx43 protein and mRNA expression. Treatment of ECs with PKA inhibitor H89 or PI3K inhibitor LY294002 prevented the AdE4+-mediated regulation of Cx40 and Cx43 that was associated with diminished AdE4+-mediated survival of ECs. Moreover, both PKA activity and cAMP-response element (CRE)-binding activity were enhanced by treatment of ECs with AdE4+. However, there is no causal evidence of a cross-talk between the 2 modulatory pathways, PKA and PI3K. Remarkably, Cx40 immunostaining was markedly increased and Cx43 was decreased in the heart tissue of mice treated with intra-tracheal AdE4+. Taken together, these results suggest that AdE4+ may play an important role in the regulation of Cx expression in ECs, and that these effects are mediated by both the PKA/CREB and PI3K signaling pathways.
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Registered trials
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