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subarachnoid hemorrhage/tyrosine
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 51 risultati
Contribution of Src tyrosine kinase to cerebral vasospasm after subarachnoid hemorrhage.
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OBJECTIVE
Mitogen-activated protein kinase (MAPK) has been implicated in cerebral vasospasm after subarachnoid hemorrhage (SAH). This study was conducted to investigate whether Src tyrosine kinase, an upstream regulator of MAPK, is involved in cerebral vasospasm.
METHODS
An established canine
Tyrosine phosphatase inhibition attenuates early brain injury after subarachnoid hemorrhage in rats.
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OBJECTIVE
Sodium orthovanadate (SOV) is a representative tyrosine phosphatase inhibitor and has been shown to ameliorate neuronal injury in cerebral ischemia. We hypothesized that tyrosine phosphatase inhibition by SOV might attenuate early brain injury after subarachnoid hemorrhage (SAH) in this
Chronological changes of the contractile mechanism in prolonged vasospasm after subarachnoid hemorrhage: from protein kinase C to protein tyrosine kinase.
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OBJECTIVE
Protein kinase C (PKC) plays a role in vasospasm after subarachnoid hemorrhage with a "two-hemorrhage" canine model until Day 7. However, clinical vasospasm continues during the course of 2 weeks. This study sought to clarify whether the contractile property of cerebral arteries might
Soluble Fms-like tyrosine kinase-1 (sFlt-1) and risk of cerebral vasospasm after aneurysmal subarachnoid hemorrhage.
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BACKGROUND
The molecular mechanisms underlying cerebral vasospasm and delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) are incompletely understood. We hypothesized that circulating antiangiogenic factors, such as soluble Fms-like tyrosine kinase 1 (sFlt-1) and soluble
Reduced tyrosine hydroxylase-like immunoreactivity around cerebral arteries after experimental subarachnoid hemorrhage in rats. An immunohistochemical study.
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In a subarachnoid hemorrhage (SAH) model of the rat, there is a decreased tyrosine hydroxylase-like immunoreactivity in the adrenergic nerves around cerebral arteries. No altered reactivity is found in the superior cervical ganglion or in the nerve bundles around the internal carotid artery of
Macrophage-Inducible C-Type Lectin/Spleen Tyrosine Kinase Signaling Pathway Contributes to Neuroinflammation After Subarachnoid Hemorrhage in Rats.
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OBJECTIVE
Macrophage-inducible C-type lectin (Mincle, CLEC4E) receptor is reported involved in neuroinflammation in cerebral ischemia and traumatic brain injury. This study was designed to investigate the role of Mincle and its downstream spleen tyrosine kinase (Syk) signal pathway in early brain
Suramin-induced reversal of chronic cerebral vasospasm in experimental subarachnoid hemorrhage.
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OBJECTIVE
The naphthylsulfonate derivative suramin is an inhibitor of growth factor receptors (receptor tyrosine kinases) and G protein-coupled P2Y receptors. Both types of these receptors are suspected of being involved in cerebral vasospasm after subarachnoid hemorrhage (SAH). In the current
Role of tyrosine kinase in fibroblast compaction and cerebral vasospasm.
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Hemolysate, a proposed causative agent for cerebral vasospasm following subarachnoid hemorrhage, produces contraction of cerebral arteries by activation of tyrosine kinases. In addition, hemolysate accelerates fibroblast collagen compaction that could play a role in cerebral vasospasm. We studied
Hemolysate induces tyrosine phosphorylation and collagen-lattice compaction in cultured fibroblasts.
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Hemolysate, a proposed causative agent for cerebral vasospasm after subarachnoid hemorrhage, produces contraction of cerebral arteries by activation of tyrosine kinases. In addition, hemolysate increases fibroblast-collagen compaction that could play a role in cerebral vasospasm. We studied the
Inhibitory effects of eicosapentaenoic acid on chronic cerebral vasospasm after subarachnoid hemorrhage: possible involvement of a sphingosylphosphorylcholine-rho-kinase pathway.
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OBJECTIVE
Rho-kinase (ROK)-mediated Ca2+ sensitization of vascular smooth muscle (VSM) contraction plays a pivotal role in cerebral vasospasm (CV). We previously demonstrated that sphingosylphosphorylcholine (SPC) induces Ca2+ sensitization through sequential activation of the Src family protein
Imatinib mesylate prevents cerebral vasospasm after subarachnoid hemorrhage via inhibiting tenascin-C expression in rats.
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Platelet-derived growth factor (PDGF) has been implicated in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH), but the mechanism remains unknown. The purpose of this study was to assess whether imatinib mesylate (imatinib), an inhibitor of the tyrosine kinases of PDGF
Preservation of tropomyosin-related kinase B (TrkB) signaling by sodium orthovanadate attenuates early brain injury after subarachnoid hemorrhage in rats.
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OBJECTIVE
Recent studies reported that apoptosis was involved in the pathogenesis of early brain injury after subarachnoid hemorrhage (SAH). The aim of this study was to examine whether sodium orthovanadate (SOV) prevents post-SAH apoptosis by modulating growth factors and its downstream receptor
Effects of tenascin-C on early brain injury after subarachnoid hemorrhage in rats.
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OBJECTIVE
We previously reported that tenascin-C (TNC), a matricellular protein, was involved in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH), but the role of TNC in early brain injury (EBI) is unknown. This study assessed whether inhibition of TNC upregulation in brain
Enhanced contractile response of the basilar artery to platelet-derived growth factor in subarachnoid hemorrhage.
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OBJECTIVE
The level of platelet-derived growth factor (PDGF) in cerebrospinal fluid is elevated in subarachnoid hemorrhage (SAH). Therefore, the contractile effect of PDGF on the basilar artery was examined in SAH.
METHODS
A rabbit double-hemorrhage SAH model was used. In the medial layers of the
Therapeutically Targeting Platelet-Derived Growth Factor-Mediated Signaling Underlying the Pathogenesis of Subarachnoid Hemorrhage-Related Vasospasm.
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BACKGROUND
Vasospasm accounts for a large fraction of the morbidity and mortality burden in patients sustaining subarachnoid hemorrhage (SAH). Platelet-derived growth factor (PDGF)-β levels rise following SAH and correlate with incidence and severity of vasospasm.
METHODS
The literature was reviewed
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