ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010
Protein kinase A phosphorylation of tau-serine 214 reorganizes microtubules and disrupts the endothelial cell barrier.
Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Complex regulation of tau phosphorylation by the endothelin system in brain microvascular endothelial cells (BMVECs): link to barrier function.Clinical science (London, England : 1979) · 2024Article
- cUMP elicits interendothelial gap formation duringAmerican journal of physiology. Lung cellular and molecular physiology · 2024Article
- Soluble pathogenic tau enters brain vascular endothelial cells and drives cellular senescence and brain microvascular dysfunction in a mouse model of tauopathy.Nature communications · 2023Article
- Developmental diversity and unique sensitivity to injury of lung endothelial subtypes during postnatal growth.iScience · 2023Article
- Identification of Novel Kinases of Tau Using Fluorescence Complementation Mass Spectrometry (FCMS).Molecular & cellular proteomics : MCP · 2022Article
- Review
- VIP modulates human macrophages phenotype via FPRL1 via activation of RhoA-GTPase and PLC pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- GSKIP-Mediated Anchoring Increases Phosphorylation of Tau by PKA but Not by GSK3beta via cAMP/PKA/GSKIP/GSK3/Tau Axis Signaling in Cerebrospinal Fluid and iPS Cells in Alzheimer Disease.Journal of clinical medicine · 2019Article
- fMLP-dependent activation of Akt and ERK1/2 through ROS/Rho A pathways is mediated through restricted activation of the FPRL1 (FPR2) receptor.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- Phosphodiesterase 10A is overexpressed in lung tumor cells and inhibitors selectively suppress growth by blocking β-catenin and MAPK signaling.Oncotarget · 2017Article
- Pitfalls in assessing microvascular endothelial barrier function: impedance-based devices versus the classic macromolecular tracer assay.Scientific reports · 2016Article
- Tau-driven 26S proteasome impairment and cognitive dysfunction can be prevented early in disease by activating cAMP-PKA signaling.Nature medicine · 2016Article
- A direct interaction between fascin and microtubules contributes to adhesion dynamics and cell migration.Journal of cell science · 2015Article
- Heterogeneity of pulmonary endothelial cyclic nucleotide response to Pseudomonas aeruginosa ExoY infection.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Monomeric C-reactive protein--a key molecule driving development of Alzheimer's disease associated with brain ischaemia?Scientific reports · 2015Article
- Tau depletion prevents progressive blood-brain barrier damage in a mouse model of tauopathy.Acta neuropathologica communications · 2015Article
- Genetic suppression of β2-adrenergic receptors ameliorates tau pathology in a mouse model of tauopathies.Human molecular genetics · 2014Article
- Cyclic AMP compartments and signaling specificity: role of cyclic nucleotide phosphodiesterases.The Journal of general physiology · 2014Article
- Article
- Pseudomonas aeruginosa exotoxin Y is a promiscuous cyclase that increases endothelial tau phosphorylation and permeability.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Intracellular cAMP is compartmentalized to near membrane domains in endothelium, where it strengthens endothelial cell barrier function. Phosphodiesterase 4D4 (PDE4D4) interacts with the spectrin membrane skeleton and prevents cAMP from accessing microtubules. Expression of a dominant-negative PDE4D4 peptide enables cAMP to access microtubules, where it results in phosphorylation of the nonneuronal microtubule-associated protein tau at serine 214. Presently, we sought to determine whether PKA is responsible for tau-Ser214 phosphorylation and furthermore whether PKA phosphorylation of tau-Ser214 is sufficient to reorganize microtubules and induce endothelial cell gaps. In cells expressing the dominant-negative PDE4D4 peptide, forskolin activated transmembrane adenylyl cyclases, increased cAMP, and induced tau-Ser214 phosphorylation that was accompanied by microtubule reorganization. PKA catalytic and regulatory I subunits, but not the regulatory II subunit, coassociated with reorganized microtubules. To determine the functional consequence of tau-Ser214 phosphorylation, wild-type human tau40 and tau40 engineered to possess an alanine point mutation (S214A) were stably expressed in endothelium. In cells expressing the dominant-negative PDE4D4 peptide and tau-S214A, PKA-dependent phosphorylation of both the endogenous and heterologously expressed tau were abolished. Expression of tau-S214A prevented forskolin from depolymerizing microtubules, inducing intercellular gaps, and increasing macromolecular permeability. These findings therefore identify nonneuronal tau as a critical cAMP-responsive microtubule-associated protein that controls microtubule architecture and endothelial cell barrier function.
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