Correction: Matrix Metalloproteinase-2 and -9 Secreted by Leukemic Cells Increase the Permeability of Blood-Brain Barrier by Disrupting Tight Junction Proteins

Feng, Saran; Cen, Jiannong; Huang, Yadong; Shen, Hongjie; Li, Yao; Wang, Yuanyuan; Chen, Zixing

doi:10.1371/annotation/716c0fb2-dbdd-4da5-ad8a-d2b1cdac4ec6

Cited by 44 publications

(18 citation statements)

References 36 publications

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“…In contrast to their wild-type littermates, MCPIP1 –/– mice developed increased FITC-dextran leakage and reduced expression of tight junction proteins claudin-5 and ZO-1 after 24 h of reperfusion following 2 h of MCAO, suggesting the BBB structural integrity and function are exacerbated by absence of MCPIP1 in mice. Both claudin-5 and ZO-1, two most widely studied components of BBB tight junction proteins, are crucial to maintain BBB homeostasis [23], and they are also vulnerable being degraded by MMPs such as MMP-3 and -9 [24,25]. Since the degradation of claudin-5 and ZO-1 are highly correlated with the dynamic process of BBB break down following cerebral ischemia [9,10,26], the reduced expression of tight junction proteins claudin-5 and ZO-1 in the MCPIP–/– mice after cerebral I/R may contribute to the BBB disruption, leading to enhanced extravasation of FITC-dextran seen in the MCPIP–/– mice (Figure 5).…”

Section: Discussionmentioning

confidence: 99%

Absence of MCP-induced Protein 1 Enhances Blood–Brain Barrier Breakdown after Experimental Stroke in Mice

Jin

Liang

et al. 2019

IJMS

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Focal cerebral ischemia can cause blood–brain barrier (BBB) breakdown, which is implicated in neuroinflammation and progression of brain damage. Monocyte chemotactic protein 1–induced protein 1 (MCPIP1) is a newly identified zinc-finger protein that negatively regulates inflammatory signaling pathways. We aimed to evaluate the impact of genetic MCPIP1 deletion on BBB breakdown and expression of BBB-related matrix metalloproteinases (MMPs) and tight junction proteins after cerebral ischemia/reperfusion (I/R) using MCPIP1-deficient (MCPIP1–/–) mice. Transient middle cerebral artery occlusion was induced in the MCPIP1–/– mice and their wild-type littermates for 2 h followed by reperfusion for 24 h. The degree of BBB breakdown was evaluated by injection of fluorescein isothiocyanate (FITC)-dextran. Quantitative real-time polymerase chain reaction, western blot, and immunohistochemistry were performed to compare the expression of MMPs and claudin-5 and zonula occludens-1 (ZO-1). MCPIP1 deficiency in mice resulted in enhanced leakage of FITC-dextran, increased expression of MMP-9/3, and reduced expression of claudin-5 and ZO-1 in the brain compared to that seen in their wild-type littermates subjected to cerebral I/R. These results demonstrate that absence of MCPIP1 exacerbates cerebral I/R-induced BBB disruption by enhancing the expression of MMP-9/3 and the degradation of claudin-5 and ZO-1, providing novel insights into the mechanisms underlying BBB breakdown after cerebral ischemia/reperfusion

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Section: Discussionmentioning

confidence: 99%

Absence of MCP-induced Protein 1 Enhances Blood–Brain Barrier Breakdown after Experimental Stroke in Mice

Jin

Liang

et al. 2019

IJMS

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“…For example, an increase in glutamate associated with seizures can lead to elevated matrix metalloproteinase (MMP)-2 and MMP-9 levels, the enzymes that regulate integrity of the extracellular matrix. Increased MMPs may then digest the tight junction proteins and increase BBB permeability [196,197,198].…”

Section: Neuroinflammatory Mechanisms Driving Ptementioning

confidence: 99%

Neuroinflammation in Post-Traumatic Epilepsy: Pathophysiology and Tractable Therapeutic Targets

et al. 2019

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Epilepsy is a common chronic consequence of traumatic brain injury (TBI), contributing to increased morbidity and mortality for survivors. As post-traumatic epilepsy (PTE) is drug-resistant in at least one-third of patients, there is a clear need for novel therapeutic strategies to prevent epilepsy from developing after TBI, or to mitigate its severity. It has long been recognized that seizure activity is associated with a local immune response, characterized by the activation of microglia and astrocytes and the release of a plethora of pro-inflammatory cytokines and chemokines. More recently, increasing evidence also supports a causal role for neuroinflammation in seizure induction and propagation, acting both directly and indirectly on neurons to promote regional hyperexcitability. In this narrative review, we focus on key aspects of the neuroinflammatory response that have been implicated in epilepsy, with a particular focus on PTE. The contributions of glial cells, blood-derived leukocytes, and the blood–brain barrier will be explored, as well as pro- and anti-inflammatory mediators. While the neuroinflammatory response to TBI appears to be largely pro-epileptogenic, further research is needed to clearly demonstrate causal relationships. This research has the potential to unveil new drug targets for PTE, and identify immune-based biomarkers for improved epilepsy prediction.

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“…Activated MMPs regulate BBB integrity, having a role in the digestion of tight junctions and BBB basement membrane proteins and are therefore critical contributors to different brain diseases [76,77]. Although MMPs play a crucial role in remodeling processes in developing and regenerating tissues, including neuronal networks in the brain [78,79], they also cleave cell surface molecules and soluble factors, such as chemokines, cytokines and their receptors [79].…”

Section: Proinflammatory Cytokine Il-18 and Hallmarks Of Alzheimermentioning

confidence: 99%

The Role of Interleukin-18, Oxidative Stress and Metabolic Syndrome in Alzheimer’s Disease

Ojala

Sutinen

2017

JCM

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The role of interleukins (ILs) and oxidative stress (OS) in precipitating neurodegenerative diseases including sporadic Alzheimer’s disease (AD), requires further clarification. In addition to neuropathological hallmarks—extracellular neuritic amyloid-β (Aβ) plaques, neurofibrillary tangles (NFT) containing hyperphosphorylated tau and neuronal loss—chronic inflammation, as well as oxidative and excitotoxic damage, are present in the AD brain. The pathological sequelae and the interaction of these events during the course of AD need further investigation. The brain is particularly sensitive to OS, due to the richness of its peroxidation-sensitive fatty acids, coupled with its high oxygen demand. At the same time, the brain lack robust antioxidant systems. Among the multiple mechanisms and triggers by which OS can accumulate, inflammatory cytokines can sustain oxidative and nitrosative stress, leading eventually to cellular damage. Understanding the consequences of inflammation and OS may clarify the initial events underlying AD, including in interaction with genetic factors. Inflammatory cytokines are potential inducers of aberrant gene expression through transcription factors. Susceptibility disorders for AD, including obesity, type-2 diabetes, cardiovascular diseases and metabolic syndrome have been linked to increases in the proinflammatory cytokine, IL-18, which also regulates multiple AD related proteins. The association of IL-18 with AD and AD-linked medical conditions are reviewed in the article. Such data indicates that an active lifestyle, coupled to a healthy diet can ameliorate inflammation and reduce the risk of sporadic AD.

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Correction: Matrix Metalloproteinase-2 and -9 Secreted by Leukemic Cells Increase the Permeability of Blood-Brain Barrier by Disrupting Tight Junction Proteins

Cited by 44 publications

References 36 publications

Absence of MCP-induced Protein 1 Enhances Blood–Brain Barrier Breakdown after Experimental Stroke in Mice

Absence of MCP-induced Protein 1 Enhances Blood–Brain Barrier Breakdown after Experimental Stroke in Mice

Neuroinflammation in Post-Traumatic Epilepsy: Pathophysiology and Tractable Therapeutic Targets

The Role of Interleukin-18, Oxidative Stress and Metabolic Syndrome in Alzheimer’s Disease

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