Recombinant Osteopontin Attenuates Brain Injury after Intracerebral Hemorrhage in Mice

Bi-hua, WU; Ma, Qingyi; Suzuki, Hitomi; Chen, Chunhua; Liu, Wenwu; Tang, Jiping; Zhang, Junyi

doi:10.1007/s12028-010-9372-z

Cited by 28 publications

(32 citation statements)

References 37 publications

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“…Recent studies have been focused on the role of OPN in central nervous system. Administration of recombinant OPN (r-OPN) attenuated intracerebral hemorrhage-induced brain injury by suppressing matrix metalloproteinase-9 (MMP-9) activity via inhibiting inducible nitric oxide synthase (iNOS) upregulation (Wu et al, 2011). Also, r-OPN has been demonstrated to prevent early brain injury (EBI) and stabilize blood brain barrier disruption by inhibiting NF-κB dependent MMP-9 induction (Suzuki et al, 2010a).…”

Section: Introductionmentioning

confidence: 99%

Recombinant osteopontin attenuates experimental cerebral vasospasm following subarachnoid hemorrhage in rats through an anti-apoptotic mechanism

Liu

et al. 2015

Brain Research

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Section: Introductionmentioning

confidence: 99%

Recombinant osteopontin attenuates experimental cerebral vasospasm following subarachnoid hemorrhage in rats through an anti-apoptotic mechanism

Liu

et al. 2015

Brain Research

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“…The OPN is induced within 3 hours of brain injury [37]. Furthermore, OPN increases cellular resistance to the damaging effects of nitric oxide and oxidative burst associated with inflammation by inhibiting the induction of nitric oxide synthase [37,38]. In a previous study, it has been shown that serum OPN levels are independently associated with a negative long-term outcome among acute ischemic stroke patients [9].…”

Section: Resultsmentioning

confidence: 99%

“…In an experimental study, it has been revealed that recombinant OPN prevented ICH-induced brain injury in terms of neurobehavioral tests, brain water content measurements, and neuronal cell count in the peri-hematoma region. The OPN is induced within 3 hours of brain injury [37]. Furthermore, OPN increases cellular resistance to the damaging effects of nitric oxide and oxidative burst associated with inflammation by inhibiting the induction of nitric oxide synthase [37,38].…”

Section: Resultsmentioning

confidence: 99%

Serum Levels of Calcification Inhibitors in Patients With Intracerebral Hemorrhage

Açar

Çevik

Arıkanoğlu

et al. 2011

International Journal of Neuroscience

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The vascular calcification regulators and inflammatory markers including fetuin-A, osteopontin (OPN), and matrix Gla protein (MGP) may play an important role in the development of intracerebral hemorrhages (ICHs). So far, the relationship between these parameters and ICH has not been studied. Therefore, this study was designed to elucidate whether fetuin-A, MGP, and OPN are involved in the pathophysiology of ICH. The ICH group consisted of 27 consecutive patients with spontaneous ICH evaluated in the neurology intensive care unit within the first 24 hours from the onset of the stroke. The serum OPN levels were significantly increased in patients with ICH compared to the controls. On the other hand, the serum MGP and fetuin-A levels were significantly decreased in the patients with ICH in comparison to the controls. In the patients with ICH, the serum MGP levels of the nonsurvivors were statistically significantly lower than the MGP levels of the survivors. In conclusion, the change in serum fetuin-A, MGP, and OPN levels after ICH indicates that these parameters play a role in the pathophysiological processes leading to an ICH. Measurement of the serum MGP levels may also be of value to estimate mortality.

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“…Extracellular matrix glycoprotein osteopontin (OPN) may offer another upstream pathway of MMP-9 regulation. In a collagenaseinduced ICH mouse model, animals pretreated with recombinant OPN 20 minutes prior to ICH induction had lower levels of MMP-9 and improved clinical outcomes [54] . OPN inhibition of MMP-9 appears to occur through down regulation of inducible nitric oxide synthase, another known activator of MMP-9 [55] .…”

Section: Transcriptional Control Of Mmp Expressionmentioning

confidence: 97%

“…Using the same combined dosing regimen, GGA treatment resulted in decreased neuronal cell death and inflammatory cell migration at 72 hours post-ICH, as well as increased neurological function after ICH induction [52] . Like PDTC and dexamethasone, GGA's effect on MMP-9 may be mediated through inhibition of NF-kB; still, the exact mechanism remains uncertain since presently available research did not directly measure MMP-9 levels in the brain [53,54] . Extracellular matrix glycoprotein osteopontin (OPN) may offer another upstream pathway of MMP-9 regulation.…”

Section: Transcriptional Control Of Mmp Expressionmentioning

confidence: 99%

Matrix Metalloproteinase Regulation in Intracerebral Hemorrhage

Chang

Jones

Betlachin

et al. 2015

International Journal of Neurology Research

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Intracerebral hemorrhage remains a particularly devastating form of cerebrovascular disease with unchanged mortality rates despite several large studies that have targeted primary expansion of hematoma growth. A second, worthwhile target for improving clinical outcome after intracerebral hemorrhage may be neuroprotection through modulation of secondary mechanisms of brain injury. Matrix metalloproteinases represent a family of ubiquitous endopeptidase enzymes that can become pathologically activated and result in blood-brain barrier breakdown. In humans, high levels of matrix metalloproteinase have been associated with perihematomal edema, symptomatic hemorrhagic transformation, and worse clinical outcome. As a result, inhibition of matrix metalloproteinase in the acute phase of intracerebral hemorrhage may represent an efficacious strategy for improving clinical outcome. Current strategies for inhibiting matrix metalloproteinase in intracerebral hemorrhage are as follows: (1) direct inhibition, (2) transcriptional control of matrix metalloproteinase expression, and (3) post-transcriptional control. Currently, the most clinically relevant form of matrix metalloproteinase inhibition lies with direct inhibition through broad-spectrum hydroxamate-class inhibitors and tetracycline-class antibiotics and the polymechanistic role of statins. Further trials are necessary to evaluate for possible roles of matrix metalloproteinase inhibition in improving clinical outcome after intracerebral hemorrhage.

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Recombinant Osteopontin Attenuates Brain Injury after Intracerebral Hemorrhage in Mice

Abstract: This study suggests that r-OPN may down-regulate iNOS expression by the inhibition of Stat1 phosphorylation, and therefore suppressing the MMP-9 activation, preventing ICH-induced brain injury in mice.

Cited by 28 publications

References 37 publications

Recombinant osteopontin attenuates experimental cerebral vasospasm following subarachnoid hemorrhage in rats through an anti-apoptotic mechanism

Recombinant osteopontin attenuates experimental cerebral vasospasm following subarachnoid hemorrhage in rats through an anti-apoptotic mechanism

Serum Levels of Calcification Inhibitors in Patients With Intracerebral Hemorrhage

Matrix Metalloproteinase Regulation in Intracerebral Hemorrhage

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