ArticleThe Journal of pharmacology and experimental therapeutics2010
Extracellular 3',5'-cAMP-adenosine pathway inhibits glomerular mesangial cell growth.
Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- DPP4 Inhibition, NPYThe Journal of pharmacology and experimental therapeutics · 2020Article
- Adenosine Receptors As Drug Targets for Treatment of Pulmonary Arterial Hypertension.Frontiers in pharmacology · 2017Review
- Purines: forgotten mediators in traumatic brain injury.Journal of neurochemistry · 2016Review
- Adenosine Attenuates Human Coronary Artery Smooth Muscle Cell Proliferation by Inhibiting Multiple Signaling Pathways That Converge on Cyclin D.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Cyclic nucleotide signalling in kidney fibrosis.International journal of molecular sciences · 2015Review
- P2X1 receptor-mediated inhibition of the proliferation of human coronary smooth muscle cells involving the transcription factor NR4A1.Purinergic signalling · 2013Article
- Endogenous production of extracellular adenosine by trabecular meshwork cells: potential role in outflow regulation.Investigative ophthalmology & visual science · 2012Article
- Extracellular 2',3'-cAMP and 3',5'-cAMP stimulate proliferation of preglomerular vascular endothelial cells and renal epithelial cells.American journal of physiology. Renal physiology · 2012Article
- The 2',3'-cAMP-adenosine pathway.American journal of physiology. Renal physiology · 2011Review
- Extracellular cAMP-adenosine pathways in the mouse kidney.American journal of physiology. Renal physiology · 2011Article
- 2'-AMP and 3'-AMP inhibit proliferation of preglomerular vascular smooth muscle cells and glomerular mesangial cells via A2B receptors.The Journal of pharmacology and experimental therapeutics · 2011Article
- Extracellular 2,3-cyclic adenosine monophosphate is a potent inhibitor of preglomerular vascular smooth muscle cell and mesangial cell growth [corrected].Hypertension (Dallas, Tex. : 1979) · 2010Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Abnormal growth of glomerular mesangial cells (GMCs) contributes to the pathophysiology of many types of nephropathy. Because adenosine is an autocrine/paracrine factor that potentially could regulate GMC proliferation and because the extracellular 3',5'-cAMP-adenosine pathway (i.e., the conversion of extracellular 3',5'-cAMP to 5'-AMP and adenosine on the cell surface) could generate adenosine in the biophase of GMC receptors, we investigated the role of the 3',5'-cAMP-adenosine pathway in modulating growth [cell proliferation, DNA synthesis ([(3)H]thymidine incorporation), collagen synthesis ([(3)H]proline incorporation), and mitogen-activated protein kinase activity] of GMCs. The addition of exogenous 3',5'-cAMP to human GMCs increased extracellular levels of 5'-AMP, adenosine, and inosine, and 3-isobutyl-1-methylxanthine (phosphodiesterase inhibitor), 1,3-dipropyl-8-p-sulfophenylxanthine (ecto-phosphodiesterase inhibitor), and alpha,beta-methylene-adenosine-5'-diphosphate (ecto-5'-nucleotidase inhibitor) attenuated the increases in adenosine and inosine. Forskolin augmented extracellular 3',5'-cAMP and adenosine concentrations, and 2',5'-dideoxyadenosine (adenylyl cyclase inhibitor) blocked these increases. Exogenous 3',5'-cAMP and forskolin inhibited all indices of cell growth, and antagonism of A(2) [(E)-8-(3,4-dimethoxystyryl)-1,3-dipropyl-7-methylxanthine, KF17837] or A(1)/A(2) (1,3-dipropyl-8-p-sulfophenylxanthine, DPSPX), but not A(1) (8-cyclopentyl-1,3-dipropylxanthine), or A(3){N-(2-methoxyphenyl)-N'-[2-(3-pyridinyl)-4-quinazolinyl]-urea, VUF5574}, adenosine receptors blocked the growth-inhibitory actions of exogenous 3',5'-cAMP, but not the effects of 8-bromo-3',5'-cAMP (stable 3',5'-cAMP analog). Erythro-9-(2-hydroxy-3-nonyl)adenine (adenosine deaminase inhibitor) plus 5-iodotubercidin (adenosine kinase inhibitor) enhanced the growth inhibition by exogenous 3',5'-cAMP and forskolin, and A(2) receptor antagonism blocked this effect. In rat GMCs, down-regulation of A(2B) receptors with antisense, but not sense or scrambled, oligonucleotides abrogated the inhibitory effects of 3',5'-cAMP and forskolin on cell growth. The extracellular 3',5'-cAMP-adenosine pathway exists in GMCs and attenuates cell growth via A(2B) receptors. Pharmacological augmentation of this pathway could abate pathological glomerular remodeling.
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