ArticleThe Journal of biological chemistry2011
Reciprocal regulation between proinflammatory cytokine-induced inducible NO synthase (iNOS) and connexin43 in bladder smooth muscle cells.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Gasotransmitters in the regulation of connexins in central and peripheral nervous system injuries.Medical gas research · 2027Review
- Review
- Construction of cancer- associated fibroblasts related risk signature based on single-cell RNA-seq and bulk RNA-seq data in bladder urothelial carcinoma.Frontiers in oncology · 2023Article
- Characterization of stanniocalcin-1 expression in macrophage differentiation.Translational oncology · 2021Article
- Sympathetic Overactivity in CKD Disrupts Buffering of Neurotransmission by Endothelium-Derived Hyperpolarizing Factor and Enhances Vasoconstriction.Journal of the American Society of Nephrology : JASN · 2020Article
- Article
- Article
- Connexin 43 plays an important role in the transformation of cholangiocytes with Clonochis sinensis excretory-secretory protein and N-nitrosodimethylamine.PLoS neglected tropical diseases · 2019Article
- Expression of Connexin 43 in Synovial Tissue of Patients With Rheumatoid Arthritis.Archives of rheumatology · 2016Article
- AMPK Suppresses Connexin43 Expression in the Bladder and Ameliorates Voiding Dysfunction in Cyclophosphamide-induced Mouse Cystitis.Scientific reports · 2016Article
- The NF-κB p65 and p50 homodimer cooperate with IRF8 to activate iNOS transcription.BMC cancer · 2015Article
- Interaction between connexin 43 and nitric oxide synthase in mice heart mitochondria.Journal of cellular and molecular medicine · 2015Article
- Vinculin directly binds zonula occludens-1 and is essential for stabilizing connexin-43-containing gap junctions in cardiac myocytes.Journal of cell science · 2014Article
- Endothelial control of vasodilation: integration of myoendothelial microdomain signalling and modulation by epoxyeicosatrienoic acids.Pflugers Archiv : European journal of physiology · 2014Review
- Myogenic bladder defects in mouse models of human oculodentodigital dysplasia.The Biochemical journal · 2014Article
- Article
- Eviprostat activates cAMP signaling pathway and suppresses bladder smooth muscle cell proliferation.International journal of molecular sciences · 2013Article
- Connexin43 hemichannel-mediated regulation of connexin43.PloS one · 2013Article
- Pannexin 1 involvement in bladder dysfunction in a multiple sclerosis model.Scientific reports · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gap junctions (GJs) play an important role in the control of bladder contractile response and in the regulation of various immune inflammatory processes. Here, we investigated the possible interaction between inflammation and GJs in bladder smooth muscle cells (BSMCs). Stimulation of BSMCs with IL1β and TNFα increased connexin43 (Cx43) expression and function, which was associated with increased phosphorylation of vasodilator-stimulated phosphoprotein. Inhibition of PKA with H89 or down-regulation of CREB with specific siRNAs largely abolished the Cx43-elevating effect. Further analysis revealed that IL1β/TNFα induced NFκB-dependent inducible NO synthase (iNOS) expression. Inhibition of iNOS with G-nitro-l-arginine methyl ester abrogated and an exogenous NO donor mimicked the effect of the cytokines on Cx43. Intraperitoneal injection of LPS into mice also induced bladder Cx43 expression, which was largely blocked by an iNOS inhibitor. Finally, the elevated Cx43 was found to negatively regulate iNOS expression. Dysfunction of GJs with various blockers or down-regulation of Cx43 with siRNA significantly potentiated the expression of iNOS. Fibroblasts from Cx43 knock-out (Cx43(-/-)) mice also displayed a significantly higher response to the cytokine-induced iNOS expression than cells from Cx43 wild-type (Cx43(+/+)) littermates. Collectively, our study revealed a previously unrecognized reciprocal regulation loop between cytokine-induced NO and GJs. Our findings may provide an important molecular mechanism for the symptoms of bladder infection. In addition, it may further our understanding of the roles of GJs in inflammatory diseases.
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