Serum S100B, brain edema, and hematoma formation in a rat model of collagenase-induced hemorrhagic stroke

Tanaka, Yu; Marumo, Toshiyuki; Shibuta, Hiromi; Omura, Tomohiro; Yoshida, Shigeru

doi:10.1016/j.brainresbull.2008.10.012

Cited by 24 publications

(12 citation statements)

References 42 publications

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“…For example, matrix metalloproteinase 9 20 and aquaporin 4 and 9 21 are upregulated in activated astrocytes and stimulate the formation of edema after ICH. Moreover, activated astrocytes release S100B into the serum, which is significantly correlated with brain edema formation and hematoma volume in ICH 22 and hemorrhagic transformation in ischemia. 23 Furthermore, ICH-associated astrocyte reactivity is increased in aged compared with young rats, 5 whereas arundic acid, a specific inhibitor of S100B synthesis, mitigates delayed infarct expansion and neurological deficits.…”

Section: Discussionmentioning

confidence: 99%

Transient Receptor Potential Canonical 3 Inhibitor Pyr3 Improves Outcomes and Attenuates Astrogliosis After Intracerebral Hemorrhage in Mice

Munakata

Shirakawa

Nagayasu

et al. 2013

Stroke

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Background and Purpose-Intracerebral hemorrhage (ICH) stems from the rupture of blood vessels in the brain, with the subsequent accumulation of blood in the parenchyma. Increasing evidence suggests that blood-derived factors induce excessive inflammatory responses that are involved in the progression of ICH-induced brain injury. Thrombin, a major bloodderived factor, leaks into the brain parenchyma on blood-brain barrier disruption and induces brain injury and astrogliosis. Furthermore, thrombin dynamically upregulates transient receptor potential canonical 3 channel, which contributes to pathological astrogliosis through a feed-forward upregulation of its own expression. The present study investigated whether Ethyl-1-(4-(2,3,3-trichloroacrylamide)phenyl)-5-(trifluoromethyl)-1H-pyrazole-4-carboxylate (Pyr3), a specific transient receptor potential canonical 3 inhibitor, can improve functional outcomes and attenuate astrogliosis after ICH in mice. Methods-Male C57BL6 mice received an intracerebral infusion of collagenase or autologous blood to induce ICH.Pyr3 was given both intracerebroventricularly and intraperitoneally after ICH induction. ICH-induced brain injury was evaluated by quantitative assessment of neurological deficits, brain swelling, and injury volume after ICH. Astrocyte activation was evaluated by immunohistochemical assessment of changes in S100 protein expression. Results-Neurological deficits, neuronal injury, brain edema, and astrocyte activation were all significantly improved by administration of Pyr3. Moreover, delayed administration of Pyr3 at 6 hours or 1 day after blood or collagenase infusion, respectively, also improved the symptoms. Conclusions-Pyr3, a specific inhibitor of transient receptor potential canonical 3, reduced the perihematomal accumulation of astrocytes and ameliorated ICH-induced brain injury. Therefore, transient receptor potential canonical 3 provides a new therapeutic target for the treatment of hemorrhagic brain injury.

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Section: Discussionmentioning

confidence: 99%

Transient Receptor Potential Canonical 3 Inhibitor Pyr3 Improves Outcomes and Attenuates Astrogliosis After Intracerebral Hemorrhage in Mice

Munakata

Shirakawa

Nagayasu

et al. 2013

Stroke

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“…Our primary aim was to simulate field administration of ROCK inhibitors by emergency medical personnel shortly after the onset of acute neurological deficits in stroke of unknown mechanism (i.e., pre‐hospital, pre‐CT). In the collagenase model of ICH, hemorrhage starts within an hour and tends to plateau within 6 h . Therefore, we chose to administer the treatments 1 h after collagenase injection.…”

Section: Discussionmentioning

confidence: 99%

Rho‐kinase inhibitors do not expand hematoma volume in acute experimental intracerebral hemorrhage

Akhter

Qin

Fischer

et al. 2018

Ann Clin Transl Neurol

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Rho‐associated kinase (ROCK) is an emerging target in acute ischemic stroke. Early pre‐hospital treatment with ROCK inhibitors may improve their efficacy, but their antithrombotic effects raise safety concerns in hemorrhagic stroke, precluding use prior to neuroimaging. Therefore, we tested whether ROCK inhibition affects the bleeding times, and worsens hematoma volume in a model of intracerebral hemorrhage (ICH) induced by intrastriatal collagenase injection in mice. Tail bleeding time was measured 1 h after treatment with isoform‐nonselective inhibitor fasudil, or ROCK2‐selective inhibitor KD025, or their vehicles. In the ICH model, treatments were administered 1 h after collagenase injection. Although KD025 but not fasudil prolonged the tail bleeding times, neither drug expanded the volume of ICH or worsened neurological deficits at 48 h compared with vehicle. Although more testing is needed in aged animals and comorbid models such as diabetes, these results suggest ROCK inhibitors may be safe for pre‐hospital administration in acute stroke.

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“…3 Baidya OP et al Int J Res Med Sci. 2014 Feb;2(1): [13][14][15] International Journal of Research in Medical Sciences | January-March 2014 | Vol 2 | Issue 1 Page 14 striated muscle, heart and kidney. S-100β is a Ca 2+ binding protein with four calcium binding sites.…”

Section: Introductionmentioning

confidence: 99%

S-100&#946; protein as a biomarker in acute hemorrhagic stroke

2014

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S-100β is a member of S-100 super family of proteins. This family of proteins is called so because they are 100% soluble in ammonium sulfate. S-100 is an acidic protein and has a molecular weight of 21 kilodalton. It consists of two subunit α chain and β chain. It is known that combination of these subunits is different from the location in human body. S-100β is located in glial cell and schwann cell, S-100αβ in glial cell, and S-100αα in ABSTRACT Acute hemorrhagic stroke, a subtype of acute stroke is one of the leading causes of death and disability throughout the world. At present, the diagnosis of acute hemorrhagic stroke is mainly based on Computer Tomography (CT) or Magnetic Resonance Imaging (MRI) but till now no biomarkers are routinely used in acute hemorrhagic stroke management. This article is a critical and descriptive review on the role of S100β protein as a biomarker in acute hemorrhagic stroke. Plasma S-100β level increases significantly in acute hemorrhagic stroke patients when compared to the normal subjects. Beside, the plasma S-100β can be correlated to the volume of hemorrhage in brain measured by plane CT scan. Plasma S-100β is an useful biomarker in acute hemorrhagic stroke and can be used for estimation of volume of hemorrhage in brain in acute hemorrhagic stroke patients. Thus, S-100β can be useful as an alternative to CT scan/MRI in diagnosis and in taking therapeutic decision in acute hemorrhagic stroke management.

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Serum S100B, brain edema, and hematoma formation in a rat model of collagenase-induced hemorrhagic stroke

Cited by 24 publications

References 42 publications

Transient Receptor Potential Canonical 3 Inhibitor Pyr3 Improves Outcomes and Attenuates Astrogliosis After Intracerebral Hemorrhage in Mice

Transient Receptor Potential Canonical 3 Inhibitor Pyr3 Improves Outcomes and Attenuates Astrogliosis After Intracerebral Hemorrhage in Mice

Rho‐kinase inhibitors do not expand hematoma volume in acute experimental intracerebral hemorrhage

S-100&#946; protein as a biomarker in acute hemorrhagic stroke

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Serum S100B, brain edema, and hematoma formation in a rat model of collagenase-induced hemorrhagic stroke

Cited by 24 publications

References 42 publications

Transient Receptor Potential Canonical 3 Inhibitor Pyr3 Improves Outcomes and Attenuates Astrogliosis After Intracerebral Hemorrhage in Mice

Transient Receptor Potential Canonical 3 Inhibitor Pyr3 Improves Outcomes and Attenuates Astrogliosis After Intracerebral Hemorrhage in Mice

Rho‐kinase inhibitors do not expand hematoma volume in acute experimental intracerebral hemorrhage

S-100&amp;#946; protein as a biomarker in acute hemorrhagic stroke

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S-100β protein as a biomarker in acute hemorrhagic stroke