ArticleScientific reports2016
AMPK Suppresses Connexin43 Expression in the Bladder and Ameliorates Voiding Dysfunction in Cyclophosphamide-induced Mouse Cystitis.
Article in Scientific reports, 2016. 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, 24 citations in OpenAlex.
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- Connexins and Glucose Metabolism in Cancer.International journal of molecular sciences · 2022Review
- Cystitis Induces Altered CREB Expression Related with Micturition Reflex.Medicina (Kaunas, Lithuania) · 2022Article
- Dose-Dependent Biphasic Action of Quetiapine on AMPK Signalling via 5-HT7 Receptor: Exploring Pathophysiology of Clinical and Adverse Effects of Quetiapine.International journal of molecular sciences · 2022Article
- Brexpiprazole Reduces 5-HT7 Receptor Function on Astroglial Transmission Systems.International journal of molecular sciences · 2022Article
- Flavonoid Nobiletin Attenuates Cyclophosphamide-Induced Cystitis in Mice through Mechanisms That Involve Inhibition of IL-1β Induced Connexin 43 Upregulation and Gap Junction Communication in Urothelial Cells.International journal of molecular sciences · 2022Article
- Distinct Effects of Escitalopram and Vortioxetine on Astroglial L-Glutamate Release Associated with Connexin43.International journal of molecular sciences · 2021Article
- HidroxAntioxidants (Basel, Switzerland) · 2021Article
- Double benefit of metformin treatment: improved bladder function in cyclophosphamide-induced cystitis and enhanced cytotoxicity in cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Urothelium-Specific Deletion of Connexin43 in the Mouse Urinary Bladder Alters Distension-Induced ATP Release and Voiding Behavior.International journal of molecular sciences · 2021Article
- Gap junctions amplify TRPV4 activation-initiated cell injury via modification of intracellular CaChannels (Austin, Tex.) · 2020Article
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- G-protein coupled receptor 64 (GPR64) acts as a tumor suppressor in endometrial cancer.BMC cancer · 2019Article
- AMPK Alters Detrusor Contractility During Emptying in Normal Bladder and Hypertrophied Bladder with Partial Bladder Outlet Obstruction via CaMKKβ.International journal of molecular sciences · 2019Article
- Apelin Ameliorates High Glucose-Induced Downregulation of Connexin 43 via AMPK-Dependent Pathway in Neonatal Rat Cardiomyocytes.Aging and disease · 2018Article
- Carbenoxolone inhibits TRPV4 channel-initiated oxidative urothelial injury and ameliorates cyclophosphamide-induced bladder dysfunction.Journal of cellular and molecular medicine · 2017Article
- Protective Effect of Thymoquinone against Cyclophosphamide-Induced Hemorrhagic Cystitis through Inhibiting DNA Damage and Upregulation of Nrf2 Expression.International journal of biological sciences · 2016Article
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder voiding dysfunction is closely related to local oxidation, inflammation, and enhanced channel activities. Given that the AMP-activated protein kinase (AMPK) has anti-oxidative, anti-inflammatory and channel-inhibiting properties, we examined whether and how AMPK affected bladder activity. AMPK activation in rat bladder smooth muscle cells (BSMCs) using three different AMPK agonists resulted in a decrease in connexin43 (Cx43) expression and function, which was associated with reduced CREB phosphorylation, Cx43 promoter activity and mRNA expression, but not Cx43 degradation. Downregulation of CREB with siRNA increased Cx43 expression. A functional analysis revealed that AMPK weakened BSMC contraction and bladder capacity. AMPK also counteracted the IL-1β- and TNFα-induced increase in Cx43 in BSMCs. In vivo administration of the AMPK agonist AICAR attenuated cyclophosphamide-initiated bladder oxidation, inflammation, Cx43 expression and voiding dysfunction. Further analysis comparing the responses of the wild-type (Cx43(+/+)) and heterozygous (Cx43(+/-)) Cx43 mice to cyclophosphamide revealed that the Cx43(+/-) mice retained a relatively normal micturition pattern compared to the Cx43(+/+) mice. Taken together, our results indicate that AMPK inhibits Cx43 in BSMCs and improves bladder activity under pathological conditions. We propose that strategies that target AMPK can be developed as novel therapeutic approaches for treating bladder dysfunction.
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