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calmodulin/accident vasculaire cérébral
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Alteration in Ca2+/calmodulin-sensitive adenylyl cyclase activity in the hippocampus of stroke-prone spontaneously hypertensive rats.
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This study examined the function of adenylyl cyclase (AC) activity in the hippocampus and cerebral cortex of the stroke-prone spontaneously hypertensive rat (SHRSP). Male SHRSP (8-week-old and 25-week-old) were used for the experiments, and age-matched Wistar-Kyoto rats (WKY) were used as a genetic
Calcium/calmodulin-dependent protein kinase kinase β is neuroprotective in stroke in aged mice.
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Stroke is a devastating neurological disease and the leading cause of long-term disability, particularly in the elderly. Calcium/calmodulin-dependent protein kinase kinase β (CaMKK β) is a major kinase activated by elevated levels of intracellular calcium. Our previous findings in young mice have
Genetic deletion of calcium/calmodulin-dependent protein kinase kinase β (CaMKK β) or CaMK IV exacerbates stroke outcomes in ovariectomized (OVXed) female mice.
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BACKGROUND
Stroke is the primary cause of long-term disability in the United States. Interestingly, mounting evidence has suggested potential sex differences in the response to stroke treatment in patients as, at least in part, distinct cell death programs may be triggered in females and males
The role of Ca2+-calmodulin stimulated protein kinase II in ischaemic stroke - A potential target for neuroprotective therapies.
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Studies in multiple experimental systems show that Ca2+-calmodulin stimulated protein kinase II (CaMKII) is a major mediator of ischaemia-induced cell death and suggest that CaMKII would be a good target for neuroprotective therapies in acute treatment of stroke. However, as CaMKII regulates many
Decreased plasma miR-335 expression in patients with acute ischemic stroke and its association with calmodulin expression.
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Objective To determine the expression and clinical significance of plasma miR-335 in patients with acute ischemic stroke (AIS) and investigate its association with calmodulin (CaM) expression. Methods Plasma miR-335 and CaM expression levels in patients with AIS and healthy controls were examined.
Inhibition of calcium/calmodulin-dependent protein kinase kinase (CaMKK) exacerbates impairment of endothelial cell and blood-brain barrier after stroke.
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Brain microvascular endothelial cells play an essential role in maintaining blood-brain barrier (BBB) integrity, and disruption of the BBB aggravates the ischemic injury. CaMKK (α and β) is a major kinase activated by elevated intracellular calcium. Previously, we demonstrated that inhibition of
Changes of calmodulin contents in single vascular smooth muscle cells from the tail arteries of spontaneously hypertensive rats.
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By combining immunohistochemistry and fluorocytometry techniques, total calmodulin (total CaM), Ca(2+)-bound calmodulin (Ca.CaM) and total protein contents in single vascular smooth muscle cells (VSMC) enzymatically dispersed from the tail arteries of young (5-7 weeks old, prehypertensive) and adult
Global forebrain ischemia results in decreased immunoreactivity of calcium/calmodulin-dependent protein kinase II.
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Previous studies utilizing crude brain homogenates have shown that forebrain ischemia results in inhibition of calcium/calmodulin-dependent protein kinase II (CaM kinase II) activity without large-scale proteolysis of the enzyme. In this report, a monoclonal antibody (1C3-3D6) directed against the
Role of calmodulin in platelet receptor function.
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Platelet glycoprotein (GP)Ib-IX-V and GPVI are unique platelet receptors that bind von Willebrand factor or collagen, respectively, and control the initial interaction of circulating platelets with the blood vessel wall in physiology (hemostasis) or pathology (heart attack or stroke). Engagement of
Calmodulin-binding proteome in the brain.
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Calcium dyshomeostasis is involved in neuropathological conditions such as traumatic brain injury (TBI), stroke, and neurodegenerative diseases. Under such conditions in the brain, calmodulin (CaM), a Ca(2+) sensor, mediates critical signaling functions through binding and regulating a diverse
Hypertrophic phenotype of cardiac calcium/calmodulin-dependent protein kinase II is reversed by angiotensin converting enzyme inhibition.
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Calcium-dependent mechanisms and the renin angiotensin system (RAS) are critically involved in the hypertrophic growth of the myocardium. The calcium/calmodulin-dependent protein kinase II (CaMKII) is a ubiquitous mediator in calcium signaling and modulates calcium handling and growth mechanisms in
Protective action by methylprednisolone, allopurinol and indomethacin against stroke-induced damage to adenylate cyclase in gerbil cerebral cortex.
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Adenylate cyclase activity was investigated in either homogenate or particulate fractions from the frontal cerebral cortex of the gerbil following five experimental conditions of bilateral ischemia. After periods of 15 min ischemia, 15 min ischemia plus 15 min of recirculation or 60 min ischemia the
Bilirubin induces a calcium-dependent inhibition of multifunctional Ca2+/calmodulin-dependent kinase II activity in vitro.
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Excessive bilirubin levels in newborn infants result in long-term neurologic deficits that remain after bilirubin levels return to normal. Much of the observed neurologic deficits can be attributed to bilirubin-induced, delayed neuronal cell death. Inhibition of calcium/calmodulin-dependent kinase
Preventive effects of the cerebral circulation improver 6,7-dimethoxy-1-(3,4-dimethoxybenzyl)-4-([4-(2-methoxyphenyl)- 1-piperazinyl]methyl)isoquinoline on stroke symptoms in stroke-prone spontaneously hypertensive rats.
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Stroke-prone spontaneously hypertensive rats (SHRSP) were treated with food admixed, 6,7-dimethoxy-1-(3,4-dimethoxybenzyl)-4-([4-(2-methoxyphenyl)-1- piperazinyl]methyl)isoquinoline (Ro 22-4839), a novel cerebral circulation improver, for a period of 15 weeks starting from 5 weeks of age at an
DY-9760e, a novel calmodulin antagonist, reduces infarction after permanent focal cerebral ischemia in rats.
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DY-9760e (3-[2-[4-(3-chloro-2-methylphenyl)-1-piperazinyl]ethyl]-5,6-dimethoxy-1-(4-imidazolylmethyl)-1H-indazole dihydrochloride 3.5 hydrate), a novel calmodulin antagonist, provides effective protection against Ca(2+) ionophore-induced cytotoxicity and brain injury induced by transient focal
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