ArticleThe Biochemical journal1996
Calcium-dependent activation of Erk-1 and Erk-2 after hypo-osmotic astrocyte swelling.
Article in The Biochemical journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 103 citations in OpenAlex.
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- Lessons on brain edema in HE: from cellular to animal models and clinical studies.Metabolic brain disease · 2024Review
- Bursting at the Seams: Molecular Mechanisms Mediating Astrocyte Swelling.International journal of molecular sciences · 2019Review
- TRPV4 and AQP4 Channels Synergistically Regulate Cell Volume and Calcium Homeostasis in Retinal Müller Glia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Hydrostatic pressure-induced release of stored calcium in cultured rat optic nerve head astrocytes.Investigative ophthalmology & visual science · 2010Article
- Inhibition of ERK and JNK decreases both osmosensitive taurine release and cell proliferation in glioma cells.Neurochemical research · 2007Article
- Functional and molecular characterization of multiple K-Cl cotransporter isoforms in corneal epithelial cells.Experimental eye research · 2007Article
- Differential dependence of regulatory volume decrease behavior in rabbit corneal epithelial cells on MAPK superfamily activation.Experimental eye research · 2007Article
- Protein tyrosine nitration in hyperammonemia and hepatic encephalopathy.Metabolic brain disease · 2005Review
- Hyperosmotically induced volume change and calcium signaling in intervertebral disk cells: the role of the actin cytoskeleton.Biophysical journal · 2002Article
- Ca2+-mediated activation of ERK in hepatocytes by norepinephrine and prostaglandin F2 alpha: role of calmodulin and Src kinases.BMC cell biology · 2002Article
- Hepatic encephalopathy as a complication of liver disease.World journal of gastroenterology · 2001Review
- Osmotic cell swelling-induced ATP release mediates the activation of extracellular signal-regulated protein kinase (Erk)-1/2 but not the activation of osmo-sensitive anion channels.The Biochemical journal · 1999Article
- Mitogenic signaling by ATP/P2Y purinergic receptors in astrocytes: involvement of a calcium-independent protein kinase C, extracellular signal-regulated protein kinase pathway distinct from the phosphatidylinositol-specific phospholipase C/calcium pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Astroglial dysfunction in hepatic encephalopathy.Metabolic brain disease · 1998Review
- Inhibition of the p44/42 MAP kinase pathway protects hippocampal neurons in a cell-culture model of seizure activity.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Article
- Osmotic swelling-induced activation of the extracellular-signal-regulated protein kinases Erk-1 and Erk-2 in intestine 407 cells involves the Ras/Raf-signalling pathway.The Biochemical journal · 1998Article
- The tyrosine kinase p56lck mediates activation of swelling-induced chloride channels in lymphocytes.The Journal of cell biology · 1998Article
- Mitogen-activated protein and tyrosine kinases in the activation of astrocyte volume-activated chloride current.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
Corrections and comments
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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
The influence of hypo-osmotic cell swelling on the activity of the mitogen-activated protein (MAP) kinases Erk-1 and Erk-2 (where Erk stands for extracellular signal-regulated protein kinase) was studied in cultured rat astrocytes. Hypo-osmotic treatment led within 10 min to an increased activity of Erk-1 and Erk-2, which became maximal at 20 min and returned to the basal level within 60 min. Moreover, exposure to hypo-osmotic conditions induced a biphasic increase in cytosolic Ca2+ concentration ([Ca2+]i): a rapid peak-like increase was followed by a sustained plateau. The absence of extracellular Ca2+ completely abolished Erk activation as well as the plateau of the [Ca2+]i response after hypo-osmotic stimulation. Application of wortmannin and agents to elevate intracellular cAMP levels also completely blocked Erk activation but were without effect on the biphasic [Ca2+]i response to hypo-osmotic treatment of the cells, suggesting a role of PtdIns 3-kinase and the Ras/Raf pathway downstream of the calcium signal. Protein kinase C (PKC) and Ca2+/calmodulin (CaM)-dependent kinases are unlikely to play a role in the hypo-osmolarity-induced signalling towards MAP kinases, as revealed by the blockage of PKC and CaM kinases. Inhibition of tyrosine kinases, pertussis-toxin- or cholera-toxin-sensitive G-proteins and phospholipase C had no effect on the [Ca2+]i response; the Erk response to hypo-osmolarity was also largely unaltered. This is different from the swelling-induced MAP kinase activation in hepatocytes, which was shown to occur via a calcium-independent but G-protein- and tyrosine kinase-dependent mechanism. Thus osmo-signalling towards MAP kinases might exhibit cell-type-specific features.
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