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Arginase I release from activated neutrophils induces peripheral immunosuppression in a murine model of stroke.

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Transient suppression of peripheral immunity is a major source of complication for patients suffering from ischemic stroke. The release of Arginase I (ArgI) from activated neutrophils has recently been associated with T-cell dysfunction in a number of pathologies. However, this pathway has not been

Effectiveness of arginase inhibitors against experimentally induced stroke.

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Stroke is a lethal disease, but it disables more than it kills. Stroke is the second leading cause of death and the most frequent cause of permanent disability in adults worldwide, with 90% of survivors having residual deficits. The pathophysiology of stroke is complex and involves a strong

The Role of Arginase 1 in Post-Stroke Immunosuppression and Ischemic Stroke Severity.

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A balanced immune system response plays an important role in acute ischemic stroke (AIS) recovery. Our laboratory has previously identified several immune-related genes, including arginase 1 (ARG1), with altered expression in human AIS patients. The neutrophil-lymphocyte ratio (NLR) may be a marker

Alteration of microRNA 340-5p and Arginase-1 Expression in Peripheral Blood Cells during Acute Ischemic Stroke.

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Acute stroke alters the systemic immune response as can be observed in peripheral blood; however, the molecular mechanism by which microRNA (miRNA) regulates target gene expression in response to acute stroke is unknown. We performed a miRNA microarray on the peripheral blood of 10 patients with

Effect of stroke on arginase expression and localization in the rat brain.

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Because arginase and nitric oxide (NO) synthases (NOS) compete to degrade l-arginine, arginase plays a crucial role in the modulation of NO production. Moreover, the arginase 1 isoform is a marker of M2 phenotype macrophages that play a key role in tissue remodeling and resolution of inflammation.

Purification of a multipotent antideath activity from bovine liver and its identification as arginase: nitric oxide-independent inhibition of neuronal apoptosis.

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Catalase is an antioxidant enzyme that has been shown to inhibit apoptotic or necrotic neuronal death induced by hydrogen peroxide. We report the purification of a contaminating antiapoptotic activity from a commercial bovine liver catalase preparation by following its ability to inhibit apoptosis

Pair housing reverses post-stroke depressive behavior in mice.

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Social isolation (SI) has been linked epidemiologically to high rates of morbidity and mortality following stroke. In contrast, strong social support enhances recovery and lowers stroke recurrence. However, the mechanism by which social support influences stroke recovery has not been adequately

A large-scale chemical screen for regulators of the arginase 1 promoter identifies the soy isoflavone daidzeinas a clinically approved small molecule that can promote neuronal protection or regeneration via a cAMP-independent pathway.

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An ideal therapeutic for stroke or spinal cord injury should promote survival and regeneration in the CNS. Arginase 1 (Arg1) has been shown to protect motor neurons from trophic factor deprivation and allow sensory neurons to overcome neurite outgrowth inhibition by myelin proteins. To identify

Is the Arginase Pathway a Novel Therapeutic Avenue for Diabetic Retinopathy?

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Diabetic retinopathy (DR) is the leading cause of blindness in working age Americans. Clinicians diagnose DR based on its characteristic vascular pathology, which is evident upon clinical exam. However, extensive research has shown that diabetes causes significant neurovascular dysfunction prior to

Alterations in the modulation of cerebrovascular tone and blood flow by nitric oxide synthases in SHRsp with stroke.

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OBJECTIVE The modulation of myogenic function and cerebral blood flow (CBF) by nitric oxide (NO) synthases (NOS) was assessed in the middle cerebral arteries (MCAs) of Kyoto Wistar stroke prone hypertensive rats (SHRsp) in relation to haemorrhagic stroke development. RESULTS MCAs were studied with a

Pharmacological hypothermia induced neurovascular protection after severe stroke of transient middle cerebral artery occlusion in mice.

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Therapeutic hypothermia is a potential protective strategy after stroke. The present study evaluated the neurovascular protective potential of pharmacological hypothermia induced by the neurotensin receptor 1 agonist HPI-201 after severe ischemic stroke. Adult C57BL/6 mice were subjected to filament

[New insights into arginase. Part II. Role in physiology and pathology].

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Arginase (amidinohydrolase, EC 3.5.3.1) is known as the last enzyme in the urea cycle in the liver, but it is also present in extrahepatic tissues. Arginase hydrolyzes L-arginine to L-ornithine and urea and its biochemical and physiological role varies depending on the organism and tissue. Besides

CD4 T cell deficiency attenuates ischemic stroke, inhibits oxidative stress, and enhances Akt/mTOR survival signaling pathways in mice

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Background: Inhibition of CD4 T cells reduces stroke-induced infarction by inhibiting neuroinflammation in the ischemic brain in experimental stroke. Nevertheless, little is known about its effects on neuronal survival signaling pathways.

Anti-inflammatory effects of ADAMTS-4 in a mouse model of ischemic stroke.

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ADAMTS-4 (a disintegrin and metalloproteinase with thrombospondin motifs type 4) is a metalloprotease capable to degrade chondroitin sulfate proteoglycans leading to cartilage destruction during arthritis or to neuroplasticity during spinal cord injury (SCI). Although ADAMTS-4 is an

Xuesaitong may protect against ischemic stroke by modulating microglial phenotypes and inhibiting neuronal cell apoptosis via the STAT3 signaling pathway.

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BACKGROUND Xuesaitong mainly comprises Panax notoginseng saponins and has shown promise in an acute ischemic stroke model; however, its effect on long-term recovery following stroke, and the related mechanisms, are unknown. The objective of this study was to investigate the long-term protective

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