ArticleBiomedical reports2017
Nitric oxide/cyclic GMP pathway mediates the endothelin-1-upregulation of adiponectin expression in rat cardiomyocytes.
Article in Biomedical reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- ET-1, MMPs, ZAG, and APN Link Reduced Ocular Perfusion to Glaucoma.Biomolecules · 2025Article
- Molecular and Biochemical Mechanisms of Cardiomyopathy Development Following Prenatal Hypoxia-Focus on the NO System.Antioxidants (Basel, Switzerland) · 2025Review
- Adiponectin secretion from cardiomyocytes produces canonical multimers and partial co-localization with calsequestrin in junctional SR.Molecular and cellular biochemistry · 2019Article
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Endothelin-1 (ET-1) serves an important role in the development of cardiac dysfunction and heart failure. ET-1 and angiotensin II (AngII) comprise a mutually reciprocal signalling network in the myocardium and serve similar or additive roles in the development of heart failure. Our previous study previously demonstrated that AngII upregulated the expression of APN in cardiomyocytes through an AngII receptor type 2/nitric oxide (NO)/cyclic GMP(cGMP)-dependent pathway. The purpose of the present study was to determine the effects of ET-1 and the additive effects of ET-1 and AngII on the gene expression and secretion of APN, and the underlying mechanisms involved. ELISA was used to determine the secretion of adiponectin (APN) and reverse transcription-quantitative polymerase chain reaction was used to evaluate the gene expression of APN. ET-1 induced APN secretion in a time- and dose-dependent manner, and induced APN secretion with AngII simultaneously, as determined via APN mRNA analyses. ETA and ETB receptors were also involved. The use of a NO synthase inhibitor and an analogue of cGMP antagonist resulted in a diminished ET-1- and/or AngII-mediated APN induction in cardiomyocytes. These results suggested that ET-1, as well as AngII, upregulated the gene expression and secretion of APN via the common NO/cGMP-mediated mechanism.
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