Deoxyhypusine hydroxylase as a novel pharmacological target for ischemic stroke via inducing a unique post-translational hypusination modification

2022 ◽  
pp. 106046
Author(s):  
Qiang Guo ◽  
Yi-Chi Zhang ◽  
Wei Wang ◽  
Yu-Qi Wang ◽  
Yang Liu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Deoxyhypusine Hydroxylase ◽  
Pharmacological Target

scholarly journals The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

2016 ◽  
Vol 36 (12) ◽  
pp. 2146-2161 ◽  
Author(s):  
Yi-Je Chen ◽  
Hai M Nguyen ◽  
Izumi Maezawa ◽  
Eva M Grössinger ◽  
April L Garing ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Adult Brain ◽  
Activated Microglia ◽  
Pharmacological Target ◽  
Cerebral Artery Occlusion

Activated microglia/macrophages significantly contribute to the secondary inflammatory damage in ischemic stroke. Cultured neonatal microglia express the K+ channels Kv1.3 and KCa3.1, both of which have been reported to be involved in microglia-mediated neuronal killing, oxidative burst and cytokine production. However, it is questionable whether neonatal cultures accurately reflect the K+ channel expression of activated microglia in the adult brain. We here subjected mice to middle cerebral artery occlusion with eight days of reperfusion and patch-clamped acutely isolated microglia/macrophages. Microglia from the infarcted area exhibited higher densities of K+ currents with the biophysical and pharmacological properties of Kv1.3, KCa3.1 and Kir2.1 than microglia from non-infarcted control brains. Similarly, immunohistochemistry on human infarcts showed strong Kv1.3 and KCa3.1 immunoreactivity on activated microglia/macrophages. We next investigated the effect of genetic deletion and pharmacological blockade of KCa3.1 in reversible middle cerebral artery occlusion. KCa3.1 −/− mice and wild-type mice treated with the KCa3.1 blocker TRAM-34 exhibited significantly smaller infarct areas on day-8 after middle cerebral artery occlusion and improved neurological deficit. Both manipulations reduced microglia/macrophage activation and brain cytokine levels. Our findings suggest KCa3.1 as a pharmacological target for ischemic stroke. Of potential, clinical relevance is that KCa3.1 blockade is still effective when initiated 12 h after the insult.

INR Rise Tied to Hemorrhage Risk After Ischemic Stroke Tx

2010 ◽  
Vol 3 (3) ◽  
pp. 18
Author(s):  
JEFF EVANS
Keyword(s):  
Ischemic Stroke ◽  
Hemorrhage Risk

Predictive value of the ankle brachial index in patients with acute ischemic stroke

VASA ◽  
2014 ◽  
Vol 43 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Konstantinos Tziomalos ◽  
Vasilios Giampatzis ◽  
Stella Bouziana ◽  
Athinodoros Pavlidis ◽  
Marianna Spanou ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Hospital Mortality ◽  
Acute Ischemic Stroke ◽  
Ankle Brachial Index ◽  
Arterial Disease ◽  
National Institutes Of Health ◽  
Limited Data ◽  
Severe Stroke ◽  
Hospital Outcome ◽  
Peripheral Arterial

Background: Peripheral arterial disease (PAD) is frequently present in patients with acute ischemic stroke. However, there are limited data regarding the association between ankle brachial index (ABI) ≤ 0.90 (which is diagnostic of PAD) or > 1.40 (suggesting calcified arteries) and the severity of stroke and in-hospital outcome in this population. We aimed to evaluate these associations in patients with acute ischemic stroke. Patients and methods: We prospectively studied 342 consecutive patients admitted for acute ischemic stroke (37.4 % males, mean age 78.8 ± 6.4 years). The severity of stroke was assessed with the National Institutes of Health Stroke Scale (NIHSS)and the modified Rankin scale (mRS) at admission. The outcome was assessed with the mRS and dependency (mRS 2 - 5) at discharge and in-hospital mortality. Results: An ABI ≤ 0.90 was present in 24.6 % of the patients whereas 68.1 % had ABI 0.91 - 1.40 and 7.3 % had ABI > 1.40. At admission, the NIHSS score did not differ between the 3 groups (10.4 ± 10.6, 8.3 ± 9.3 and 9.3 ± 9.4, respectively). The mRS score was also comparable in the 3 groups (3.6 ± 1.7, 3.1 ± 1.8 and 3.5 ± 2.3, respectively). At discharge, the mRS score did not differ between the 3 groups (2.9 ± 2.2, 2.3 ± 2.1 and 2.7 ± 2.5, respectively) and dependency rates were also comparable (59.5, 47.6 and 53.3 %, respectively). In-hospital mortality was almost two-times higher in patients with ABI ≤ 0.90 than in patients with ABI 0.91 - 1.40 or > 1.40 but this difference was not significant (10.9, 6.6 and 6.3 %, respectively). Conclusions: An ABI ≤ 0.90 or > 1.40 does not appear to be associated with more severe stroke or worse in-hospital outcome in patients with acute ischemic stroke.

Benefits of abciximab for patients with ischemic stroke

2005 ◽  
Vol 2 (12) ◽  
pp. 615-615
Author(s):  
Claire Braybrook
Keyword(s):  
Ischemic Stroke

Adiposity Labeled a Risk Factor for Ischemic Stroke

2007 ◽  
Vol 37 (20) ◽  
pp. 14
Author(s):  
BRUCE JANCIN
Keyword(s):  
Risk Factor ◽  
Ischemic Stroke
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