ArticleThe Journal of physiology2005
The protein kinase MEK1/2 mediate vascular endothelial growth factor- and histamine-induced hyperpermeability in porcine coronary venules.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 59 citations in OpenAlex.
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- Circulating small extracellular vesicles mediate vascular hyperpermeability in diabetes.Diabetologia · 2024Article
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- NRP1 interacts with endoglin and VEGFR2 to modulate VEGF signaling and endothelial cell sprouting.Communications biology · 2024Article
- The Role and Therapeutic Implications of Inflammation in the Pathogenesis of Brain Arteriovenous Malformations.Biomedicines · 2023Review
- Edema and lymphatic clearance: molecular mechanisms and ongoing challenges.Clinical science (London, England : 1979) · 2023Review
- Cellular mechanisms underlying the impairment of macrophage efferocytosis.Immunology letters · 2023Review
- Growth Hormone-Releasing Hormone in Endothelial Inflammation.Endocrinology · 2022Review
- Lactate induces vascular permeability via disruption of VE-cadherin in endothelial cells during sepsis.Science advances · 2022Article
- A narrative review of changes in microvascular permeability after burn.Annals of translational medicine · 2021Review
- Myogenic tone contributes to the regulation of permeability in mesenteric microvessels.Microvascular research · 2019Article
- GHRH antagonists support lung endothelial barrier function.Tissue barriers · 2019Article
- Polarised VEGFA Signalling at Vascular Blood–Neural Barriers.International journal of molecular sciences · 2018Review
- Endothelial Protrusions in Junctional Integrity and Barrier Function.Current topics in membranes · 2018Article
- Efficient Promotion of Autophagy and Angiogenesis Using Mesenchymal Stem Cell Therapy Enhanced by the Low-Energy Shock Waves in the Treatment of Erectile Dysfunction.Stem cells international · 2018Article
- Histamine activates p38 MAP kinase and alters local lamellipodia dynamics, reducing endothelial barrier integrity and eliciting central movement of actin fibers.American journal of physiology. Cell physiology · 2015Article
- Involvement of the H1 Histamine Receptor, p38 MAP Kinase, Myosin Light Chains Kinase, and Rho/ROCK in Histamine-Induced Endothelial Barrier Dysfunction.Microcirculation (New York, N.Y. : 1994) · 2015Article
- Stromal interaction molecule 1 (STIM1) and Orai1 mediate histamine-evoked calcium entry and nuclear factor of activated T-cells (NFAT) signaling in human umbilical vein endothelial cells.The Journal of biological chemistry · 2014Article
- Myosin light chain kinase signaling in endothelial barrier dysfunction.Medicinal research reviews · 2013Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitogen-activated protein kinases (MAPKs) have been implicated in the signal transduction of the endothelial response to growth factors and inflammatory stimuli. The objective of this study was to test the hypothesis that the p42/44 MAPK pathway plays a common role in mediating the microvascular hyperpermeability response to vascular endothelial growth factor (VEGF) and histamine. The apparent permeability coefficient of albumin was measured in isolated and perfused coronary venules. Application of VEGF induced a rapid increase in venular permeability, and the effect was blocked by PD98059 and UO126, selective inhibitors of the mitogen-activated protein kinase kinase MEK1/2, in a dose-dependent pattern. The same MEK1/2 inhibitors dose-dependently attenuated the increase in venular permeability caused by histamine. In addition, the increases in venular permeability caused by agents that are known to activate the nitric oxide pathway, including the calcium ionophore ionomycin, the nitric oxide donor S-nitroso-N-acetylpenicillamine, and the protein kinase G activator 8-bromo-cGMP, were significantly attenuated in venules pretreated with the MEK1/2 inhibitors. Furthermore, transfection of venules with active MEK1 increased baseline permeability. In contrast, transfection of active ERK1, a downstream target of MEK1/2, did not significantly alter the basal permeability of venules. Moreover, inhibition of ERK1/2 with a specific inhibiting peptide did not prevent the hyperpermeability response to VEGF or histamine. The results suggest that activation of MEK1/2 may play a central role in the signal transduction of microvascular hyperpermeability in response to growth factors and inflammatory mediators.
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