ArticleJournal of neuroinflammation2014
CaMKII and MEK1/2 inhibition time-dependently modify inflammatory signaling in rat cerebral arteries during organ culture.
Article in Journal of neuroinflammation, 2014. 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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13 citing papers in PubMed, 17 citations in OpenAlex.
- Switching Off Vascular MAPK Signaling: A Novel Strategy to Prevent Delayed Cerebral Ischemia Following Subarachnoid Hemorrhage.Translational stroke research · 2025Review
- The Effect of SERCA Activation on Functional Characteristics and Signaling of Rat Soleus Muscle upon 7 Days of Unloading.Biomolecules · 2023Article
- Adeno-Associated Viruses for Modeling Neurological Diseases in Animals: Achievements and Prospects.Biomedicines · 2022Review
- Calcium/Calmodulin-Dependent Protein Kinase II in Cerebrovascular Diseases.Translational stroke research · 2021Review
- RepSox effectively promotes the induced differentiation of sheep fibroblasts into adipocytes via the inhibition of the TGF‑β1/Smad pathway.International journal of molecular medicine · 2021Article
- Activation of CaBulletin of experimental biology and medicine · 2021Article
- Multiple functions of reversine on the biological characteristics of sheep fibroblasts.Scientific reports · 2021Article
- Arsenic is more potent than cadmium or manganese in disrupting the INS-1 beta cell microRNA landscape.Archives of toxicology · 2019Article
- Hippocampal CA1 βCaMKII mediates neuroinflammatory responses via COX-2/PGE2 signaling pathways in depression.Journal of neuroinflammation · 2018Article
- IGF-1-Involved Negative Feedback of NR2B NMDA Subunits Protects Cultured Hippocampal Neurons Against NMDA-Induced Excitotoxicity.Molecular neurobiology · 2017Article
- Age-dependent alterations to paraventricular nucleus insulin-like growth factor 1 receptor as a possible link between sympathoexcitation and inflammation.Journal of neurochemistry · 2016Article
- Reversine Increases the Plasticity of Long-Term Cryopreserved Fibroblasts to Multipotent Progenitor Cells through Activation of Oct4.International journal of biological sciences · 2016Article
- CaMKII inhibition with KN93 attenuates endothelin and serotonin receptor-mediated vasoconstriction and prevents subarachnoid hemorrhage-induced deficits in sensorimotor function.Journal of neuroinflammation · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCerebral ischemia induces transcriptional upregulation of inflammatory genes in the brain parenchyma and in cerebral arteries, thereby contributing to the infarct development. The present study was designed to evaluate the involvement of calcium-calmodulin-dependent protein kinase (CaMKII) II and extracellular signal-regulated kinase1/2 (ERK1/2) on inflammatory mediators in rat cerebral arteries using organ culture as a method for inducing ischemic-like vascular wall changes.
methodsRat basilar arteries were cultured in serum-free medium for 0, 3, 6 or 24 hours in the presence or absence of the CaMKII inhibitor KN93 or the MEK1/2 inhibitor U0126. Protein expression of activated CaMKII, ERK1/2, and inflammatory-associated protein kinases and mediators were examined with western blot and immunohistochemistry. Caspase-3 mRNA levels in basilar arteries were studied with real-time PCR.
resultsWestern blot evaluation showed that organ culture induced a significant increase in phosphorylated ERK1/2 at 3, 6 and 24 hours, while CaMKII was found to be already activated in fresh non-incubated arteries and to decrease with incubation time. The addition of U0126 or KN93 decreased levels of phosphorylated c-Jun N-terminal kinase and p-p38, as evaluated by immunohistochemistry. KN93 affected the increase in caspase-3 mRNA expression only when given at the start of incubation, while U0126 had an inhibitory effect when given up to six hours later. Tumor necrosis factor receptor 1 was elevated after organ culture. This inflammatory marker was reduced by both of the two different protein kinase inhibitors.
conclusionsThe novel findings of the present study are that the cross-talk between the two protein kinases and the inhibition of CaMKII or MEK1/2 in a time-dependent manner attenuates inflammatory-associated protein kinases and mediators, suggesting that they play a role in cerebrovascular inflammation.
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