ArticleBMC neuroscience2011
Human cerebrovascular contractile receptors are upregulated via a B-Raf/MEK/ERK-sensitive signaling pathway.
Article in BMC neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Switching Off Vascular MAPK Signaling: A Novel Strategy to Prevent Delayed Cerebral Ischemia Following Subarachnoid Hemorrhage.Translational stroke research · 2025Review
- Independent and synergistic roles of MEK-ERK1/2 and PKC pathways in regulating functional changes in vascular tissue following flow cessation.Journal of molecular and cellular cardiology plus · 2025Article
- Doxorubicin alters G-protein coupled receptor-mediated vasocontraction in rat coronary arteries.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Dabrafenib, an inhibitor of RIP3 kinase-dependent necroptosis, reduces ischemic brain injury.Neural regeneration research · 2018Article
- The extracellular signal-regulated kinase 1/2 pathway in neurological diseases: A potential therapeutic target (Review).International journal of molecular medicine · 2017Review
- The Mitogen-Activated Protein Kinase (MAPK) Signaling Pathway as a Discovery Target in Stroke.Journal of molecular neuroscience : MN · 2016Review
- U0126 attenuates cerebral vasoconstriction and improves long-term neurologic outcome after stroke in female rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Article
- Regulatory mechanism of endothelin receptor B in the cerebral arteries after focal cerebral ischemia.PloS one · 2014Article
- Male-female differences in upregulation of vasoconstrictor responses in human cerebral arteries.PloS one · 2013Article
- Vascular endothelin receptor type B: structure, function and dysregulation in vascular disease.Biochemical pharmacology · 2012Review
- Effects of angiotensin II on the cerebral circulation: role of oxidative stress.Frontiers in physiology · 2012Article
- Inhibition of cerebrovascular raf activation attenuates cerebral blood flow and prevents upregulation of contractile receptors after subarachnoid hemorrhage.BMC neuroscience · 2011Article
- Vascular plasticity in cerebrovascular disorders.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011Review
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundCerebral ischemia results in a rapid increase in contractile cerebrovascular receptors, such as the 5-hydroxytryptamine type 1B (5-HT₁(B)), angiotensin II type 1 (AT₁), and endothelin type B (ET(B)) receptors, in the vessel walls within the ischemic region, which further impairs local blood flow and aggravates tissue damage. This receptor upregulation occurs via activation of the mitogen-activated protein kinase pathway. We therefore hypothesized an important role for B-Raf, the first signaling molecule in the pathway. To test our hypothesis, human cerebral arteries were incubated at 37°C for 48 h in the absence or presence of a B-Raf inhibitor: SB-386023 or SB-590885. Contractile properties were evaluated in a myograph and protein expression of the individual receptors and activated phosphorylated B-Raf (p-B-Raf) was evaluated immunohistochemically.
results5-HT₁(B), AT₁, and ET(B) receptor-mediated contractions were significantly reduced by application of SB-590885, and to a smaller extent by SB-386023. A marked reduction in AT₁ receptor immunoreactivity was observed after treatment with SB-590885. Treatment with SB-590885 and SB-386023 diminished the culture-induced increase of p-B-Raf immunoreactivity.
conclusionsB-Raf signaling has a key function in the altered expression of vascular contractile receptors observed after organ culture. Therefore, specific targeting of B-Raf might be a novel approach to reduce tissue damage after cerebral ischemia by preventing the previously observed upregulation of contractile receptors in smooth muscle cells.
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