ArticleAmerican journal of physiology. Cell physiology2007
Cellular mechanisms underlying prostaglandin-induced transient cAMP signals near the plasma membrane of HEK-293 cells.
Article in American journal of physiology. Cell physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 64 citations in OpenAlex.
- Elastogenesis in Focus: Navigating Elastic Fibers Synthesis for Advanced Dermal Biomaterial Formulation.Advanced healthcare materials · 2024Review
- GPCR Signaling Measurement and Drug Profiling with an Automated Live-Cell Microscopy System.ACS sensors · 2023Article
- Computational investigation of the dynamic control of cAMP signaling by PDE4 isoform types.Biophysical journal · 2022Article
- Ion Channel-Based Reporters for cAMP Detection.Methods in molecular biology (Clifton, N.J.) · 2022Article
- PDE-Mediated Cyclic Nucleotide Compartmentation in Vascular Smooth Muscle Cells: From Basic to a Clinical Perspective.Journal of cardiovascular development and disease · 2021Review
- A three-dimensional finite element model of cAMP signals.Forces in mechanics · 2021Article
- Chorea-related mutations in PDE10A result in aberrant compartmentalization and functionality of the enzyme.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- A two-dimensional finite element model of cyclic adenosine monophosphate (cAMP) intracellular signaling.SN applied sciences · 2019Article
- Compartmentalized cAMP Signaling Associated With Lipid Raft and Non-raft Membrane Domains in Adult Ventricular Myocytes.Frontiers in pharmacology · 2018Article
- Activation of PKA in cell requires higher concentration of cAMP than in vitro: implications for compartmentalization of cAMP signalling.Scientific reports · 2017Article
- The resolution of acute inflammation induced by cyclic AMP is dependent on annexin A1.The Journal of biological chemistry · 2017Article
- A Computational Modeling and Simulation Approach to Investigate Mechanisms of Subcellular cAMP Compartmentation.PLoS computational biology · 2016Article
- Estimating the magnitude of near-membrane PDE4 activity in living cells.American journal of physiology. Cell physiology · 2015Article
- Apremilast, a novel phosphodiesterase 4 (PDE4) inhibitor, regulates inflammation through multiple cAMP downstream effectors.Arthritis research & therapy · 2015Article
- The genetically encoded tool set for investigating cAMP: more than the sum of its parts.Frontiers in pharmacology · 2015Review
- Inactivation of the Carney complex gene 1 (PRKAR1A) alters spatiotemporal regulation of cAMP and cAMP-dependent protein kinase: a study using genetically encoded FRET-based reporters.Human molecular genetics · 2014Article
- Mechanisms of cyclic AMP compartmentation revealed by computational models.The Journal of general physiology · 2014Article
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- Cyclic AMP compartments and signaling specificity: role of cyclic nucleotide phosphodiesterases.The Journal of general physiology · 2014Article
- A-kinase anchoring proteins regulate compartmentalized cAMP signaling in airway smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
We have previously used cyclic nucleotide-gated (CNG) channels as sensors to measure cAMP signals in human embryonic kidney (HEK)-293 cells. We found that prostaglandin E(1) (PGE(1)) triggered transient increases in cAMP concentration near the plasma membrane, whereas total cAMP levels rose to a steady plateau over the same time course. In addition, we presented evidence that the decline in the near-membrane cAMP levels was due primarily to a PGE(1)-induced stimulation of phosphodiesterase (PDE) activity, and that the differences between near-membrane and total cAMP levels were largely due to diffusional barriers and differential PDE activity. Here, we examine the mechanisms regulating transient, near-membrane cAMP signals. We observed that 5-min stimulation of HEK-293 cells with prostaglandins triggered a two- to threefold increase in PDE4 activity. Extracellular application of H89 (a PKA inhibitor) inhibited stimulation of PDE4 activity. Similarly, when we used CNG channels to monitor cAMP signals we found that both extracellular and intracellular (via the whole-cell patch pipette) application of H89, or the highly selective PKA inhibitor, PKI, prevented the decline in prostaglandin-induced responses. Following pretreatment with rolipram (a PDE4 inhibitor), H89 had little or no effect on near-membrane or total cAMP levels. Furthermore, disrupting the subcellular localization of PKA with the A-kinase anchoring protein (AKAP) disruptor Ht31 prevented the decline in the transient response. Based on these data we developed a plausible kinetic model that describes prostaglandin-induced cAMP signals. This model has allowed us to quantitatively demonstrate the importance of PKA-mediated stimulation of PDE4 activity in shaping near-membrane cAMP signals.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.