Cytokine MIF Enhances Blood-Brain Barrier Permeability: Impact for Therapy in Ischemic Stroke

Liu, Yu Chuan; Tsai, Yung-Hsu; Tang, Sung‐Chun; Liou, Houng Chi; Kang, Kai-Hsiang; Liou, Horng Huei; Jeng, Jiann‐Shing; Fu, Wen

doi:10.1038/s41598-017-16927-9

Cited by 44 publications

(56 citation statements)

References 37 publications

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“…It has been shown to promote leukocyte‐endothelial cell interactions through promoting endothelial adhesion molecule expression . It has recently been suggested to directly degrade the BBB after ischemic brain . Perivascular microglia/macrophages migrate toward the disrupted blood vessels and further damage them by phagocytizing ECs .…”

Section: The Double‐faced Roles Of Peripheral Immune Activation On Thmentioning

confidence: 99%

The peripheral immune response after stroke—A double edge sword for blood‐brain barrier integrity

Zhu

Huang

et al. 2018

CNS Neurosci Ther

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Summary The blood‐brain barrier (BBB) is a highly regulated interface that separates the peripheral circulation and the brain. It plays a vital role in regulating the trafficking of solutes, fluid, and cells at the blood‐brain interface and maintaining the homeostasis of brain microenvironment for normal neuronal activity. Growing evidence has led to the realization that ischemic stroke elicits profound immune responses in the circulation and the activation of multiple subsets of immune cells, which in turn affect both the early disruption and the later repair of the BBB after stroke. Distinct phenotypes or subsets of peripheral immune cells along with diverse intracellular mechanisms contribute to the dynamic changes of BBB integrity after stroke. This review focuses on the interaction between the peripheral immune cells and the BBB after ischemic stroke. Understanding their reciprocal interaction may generate new directions for stroke research and may also drive the innovation of easy accessible immune modulatory treatment strategies targeting BBB in the pursuit of better stroke recovery.

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Section: The Double‐faced Roles Of Peripheral Immune Activation On Thmentioning

confidence: 99%

The peripheral immune response after stroke—A double edge sword for blood‐brain barrier integrity

Zhu

Huang

et al. 2018

CNS Neurosci Ther

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“…Besides, miR-186-5p is previously reported to serve as a circulating biomarker of cardiovascular risk and facilitate the diagnosis of acute coronary syndrome 6 , 15 . As reported, blood-brain barrier (BBB) was destroyed and its permeability was enhanced in ischemic stroke 16 , 17 . Thus, more small molecule materials can go through BBB and go into blood circulation.…”

Section: Discussionmentioning

confidence: 82%

miR-186-5p Promotes Apoptosis by Targeting IGF-1 in SH-SY5Y OGD/R Model

et al. 2018

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In recent years, accumulating evidence has revealed that microRNAs play critical roles in ischemia stroke. This study was designed to investigate the expression level and effects of microRNA (miR)-186-5p on ischemia stroke, and its underlying molecular mechanism. Firstly, we demonstrated that miR-186-5p were significantly up-regulated and induced apoptosis in oxygen and glucose deprivation/reperfusion (OGD/R) model. Moreover, we found that miR-186-5p reduced the expression of insulin-like growth factor (IGF)-1, an essential factor for the development of the nervous system. Meanwhile, miR-186-5p inhibitor enhanced cell viability and IGF-1 expression. Furthermore, IGF-1 was confirmed as a direct target gene of miR-186-5p by luciferase activity assay. In addition, miR-186-5p was upregulated in ischemia stroke patients' serum compared with healthy donors. These data demonstrated that miR-186-5p was an adverse factor by inducing neuron apoptosis and suppressing IGF-1 in ischemia stroke model, and suggested that miR-186-5p may be a diagnostic marker and potential therapeutic target for ischemia stroke patients.

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“…The fact that ISO1 has been shown to influence astrocytes in animal models suggest that it can cross the blood brain barrier (BBB). Interestingly, MIF has been shown to increase BBB permeability and vascular leakage, whereas ISO-1 inhibits these effects [ 40 , 61 ]. Still, studies are needed to directly assess the ability of ISO1 to penetrate into the brain.…”

Section: Discussionmentioning

confidence: 99%

“…MIF inhibition has been shown to be neuroprotective in CNS disorders such as stroke [ 39 , 40 ], and MIF interaction with the CD74 receptor has been shown to activate astrocyte responses [ 41 ]. MIF-binding to CD74 can be inhibited by administration of the small molecule ISO1 [ 42 , 43 ].…”

Section: Introductionmentioning

confidence: 99%

Antagonism of Macrophage Migration Inhibitory Factory (MIF) after Traumatic Brain Injury Ameliorates Astrocytosis and Peripheral Lymphocyte Activation and Expansion

Newell‐Rogers

Rogers

Tobin

et al. 2020

IJMS

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Traumatic brain injury (TBI) precedes the onset of epilepsy in up to 15–20% of symptomatic epilepsies and up to 5% of all epilepsy. Treatment of acquired epilepsies, including post-traumatic epilepsy (PTE), presents clinical challenges, including frequent resistance to anti-epileptic therapies. Considering that over 1.6 million Americans present with a TBI each year, PTE is an urgent clinical problem. Neuroinflammation is thought to play a major causative role in many of the post-traumatic syndromes, including PTE. Increasing evidence suggests that neuroinflammation facilitates and potentially contributes to seizure induction and propagation. The inflammatory cytokine, macrophage migration inhibitory factor (MIF), is elevated after TBI and higher levels of MIF correlate with worse post-traumatic outcomes. MIF was recently demonstrated to directly alter the firing dynamics of CA1 pyramidal neurons in the hippocampus, a structure critically involved in many types of seizures. We hypothesized that antagonizing MIF after TBI would be anti-inflammatory, anti-neuroinflammatory and neuroprotective. The results show that administering the MIF antagonist ISO1 at 30 min after TBI prevented astrocytosis but was not neuroprotective in the peri-lesion cortex. The results also show that ISO1 inhibited the TBI-induced increase in γδT cells in the gut, and the percent of B cells infiltrating into the brain. The ISO1 treatment also increased this population of B cells in the spleen. These findings are discussed with an eye towards their therapeutic potential for post-traumatic syndromes, including PTE.

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Cytokine MIF Enhances Blood-Brain Barrier Permeability: Impact for Therapy in Ischemic Stroke

Cited by 44 publications

References 37 publications

The peripheral immune response after stroke—A double edge sword for blood‐brain barrier integrity

The peripheral immune response after stroke—A double edge sword for blood‐brain barrier integrity

miR-186-5p Promotes Apoptosis by Targeting IGF-1 in SH-SY5Y OGD/R Model

Antagonism of Macrophage Migration Inhibitory Factory (MIF) after Traumatic Brain Injury Ameliorates Astrocytosis and Peripheral Lymphocyte Activation and Expansion

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