ETB receptor-mediated MMP-9 activation induces vasogenic edema via ZO-1 protein degradation following status epilepticus

Kim, J.Y.; Ko, Ah-Reum; Hyun, Hye-Won; Kang, Tae‐Cheon

doi:10.1016/j.neuroscience.2015.07.065

Cited by 49 publications

(33 citation statements)

References 57 publications

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“…Recently, it was demonstrated that the expression and localization of tight junction proteins which are responsible for the BBB integrity, such as ZO-1, are altered after SE, and that these changes were mediated by MMP-9 activity [38]. Here, we showed that ZO-1 staining is absent in the ischemic lesion and that the area of the lesion is reduced after MMP-12 inhibition, suggesting an attenuation of ZO-1 degradation.…”

Section: Discussionsupporting

confidence: 49%

A Hydroxypyrone-Based Inhibitor of Metalloproteinase-12 Displays Neuroprotective Properties in Both Status Epilepticus and Optic Nerve Crush Animal Models

Vinet

Costa

Salinas‐Navarro

et al. 2018

IJMS

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Recently, we showed that matrix metalloproteinase-12 (MMP-12) is highly expressed in microglia and myeloid infiltrates, which are presumably involved in blood–brain barrier (BBB) leakage and subsequent neuronal cell death that follows status epilepticus (SE). Here, we assessed the effects of a hydroxypyrone-based inhibitor selective for MMP-12 in the pilocarpine-induced SE rat model to determine hippocampal cell survival. In the hippocampus of rats treated with pilocarpine, intra-hippocampal injections of the MMP-12 inhibitor protected Cornu Ammonis 3 (CA3) and hilus of dentate gyrus neurons against cell death and limited the development of the ischemic-like lesion that typically develops in the CA3 stratum lacunosum-moleculare of the hippocampus. Furthermore, we showed that MMP-12 inhibition limited immunoglobulin G and albumin extravasation after SE, suggesting a reduction in BBB leakage. Finally, to rule out any possible involvement of seizure modulation in the neuroprotective effects of MMP-12 inhibition, neuroprotection was also observed in the retina of treated animals after optic nerve crush. Overall, these results support the hypothesis that MMP-12 inhibition can directly counteract neuronal cell death and that the specific hydroxypyrone-based inhibitor used in this study could be a potential therapeutic agent against neurological diseases/disorders characterized by an important inflammatory response and/or neuronal cell loss.

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Section: Discussionsupporting

confidence: 49%

A Hydroxypyrone-Based Inhibitor of Metalloproteinase-12 Displays Neuroprotective Properties in Both Status Epilepticus and Optic Nerve Crush Animal Models

Vinet

Costa

Salinas‐Navarro

et al. 2018

IJMS

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“…Despite that some astrocyte-derived factors maintain the BBB function, some astrocyte-derived factors damage the BBB by inducing endothelial cell apoptosis or decreasing the expression of endothelial tight junctionrelated proteins, which include vascular endothelial growth factor (VEGF) [204][205][206][207], glutamate [208][209][210], endothelins (ETs) [21,211,212], MMP [208,213,214], and nitric oxide (NO) [215,216] (Table 1). As zincendopeptidases, MMPs can directly degrade endothelial tight junction-related proteins and ECM molecules, which promotes angiogenesis whereas simultaneously increases BBB permeability [78,217,218].…”

Section: The Bbb Integrity-suppressing Effects Of Astrocytesmentioning

confidence: 99%

Dual roles of astrocytes in plasticity and reconstruction after traumatic brain injury

et al. 2020

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Traumatic brain injury (TBI) is one of the leading causes of fatality and disability worldwide. Despite its high prevalence, effective treatment strategies for TBI are limited. Traumatic brain injury induces structural and functional alterations of astrocytes, the most abundant cell type in the brain. As a way of coping with the trauma, astrocytes respond in diverse mechanisms that result in reactive astrogliosis. Astrocytes are involved in the physiopathologic mechanisms of TBI in an extensive and sophisticated manner. Notably, astrocytes have dual roles in TBI, and some astrocyte-derived factors have double and opposite properties. Thus, the suppression or promotion of reactive astrogliosis does not have a substantial curative effect. In contrast, selective stimulation of the beneficial astrocytederived molecules and simultaneous attenuation of the deleterious factors based on the spatiotemporalenvironment can provide a promising astrocyte-targeting therapeutic strategy. In the current review, we describe for the first time the specific dual roles of astrocytes in neuronal plasticity and reconstruction, including neurogenesis, synaptogenesis, angiogenesis, repair of the blood-brain barrier, and glial scar formation after TBI. We have also classified astrocyte-derived factors depending on their neuroprotective and neurotoxic roles to design more appropriate targeted therapies.

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“…Our data clearly suggest that the expression of MMP-9 in the model group significantly increased, and TWOD suppressed the excessive expression of MMP-9. Occluding and claudin expressions at the transcriptional level, the protein levels, and intracellular distribution were subject to the regulation of MMPs [18]. After induction by hyperglycemia, MMP-9 degraded the extracellular matrix, collagen IV, basement membrane, and TJ protein and enhanced BRB permeability [19, 20].…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Tang Wang One Decoction on the Retinal Vessels of Diabetic Rats

Kou

Yang

Qin

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Objective. This study aimed to determine the influence of Tang Wang One Decoction (TWOD) on the retinal vessels of diabetic rats. Methods. The hemorheology of diabetic rats was observed. Morphological studies of retinal vessels were conducted using optical microscopy and electron microscopy. Immunological histochemistry assay was used to measure the expression levels of MMP-9, occludin, and claudin-5. Results. Obvious pathological damage was observed in the retinal vessels of diabetic rats. TWOD positively affected the hemorheology and morphology of retinal vessels. The decoction also decreased the expression of MMP-9 and increased the expression of occludin and claudin-5. Conclusions. The results suggest that the retinal protective effects of TWOD might be related to downregulation of MMP-9 and upregulation of occludin and claudin-5.

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ETB receptor-mediated MMP-9 activation induces vasogenic edema via ZO-1 protein degradation following status epilepticus

Cited by 49 publications

References 57 publications

A Hydroxypyrone-Based Inhibitor of Metalloproteinase-12 Displays Neuroprotective Properties in Both Status Epilepticus and Optic Nerve Crush Animal Models

A Hydroxypyrone-Based Inhibitor of Metalloproteinase-12 Displays Neuroprotective Properties in Both Status Epilepticus and Optic Nerve Crush Animal Models

Dual roles of astrocytes in plasticity and reconstruction after traumatic brain injury

Protective Effect of Tang Wang One Decoction on the Retinal Vessels of Diabetic Rats

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