Inflammation at the blood-brain barrier: The role of liver X receptors

Wit, Nienke M. de; Vanmol, Jasmine; Kamermans, Alwin; Hendriks, Jerome J. A.; Vries, Helga E. de

doi:10.1016/j.nbd.2016.09.015

Cited by 24 publications

(20 citation statements)

References 112 publications

(127 reference statements)

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“…Blood-brain barrier (BBB) that regulates the solute flux plays a crucial role in the maintenance of brain homeostasis. 6 Systemic inflammation implicates and disrupts the BBB, and the dysfunction of BBB is reported as a biomarker for epileptogenesis. 7,8 Mounting evidence ascribes the precipitation and recurrence of seizures to the inflammation in the cerebral parenchyma.…”

mentioning

confidence: 99%

Retracted: MicroRNA‐132 attenuates LPS‐induced inflammatory injury by targeting TRAF6 in neuronal cell line HT‐22

Wang

Liu

et al. 2018

J of Cellular Biochemistry

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Epilepsy is a common neurological disorder in the central nervous system. Inflammation disrupts the blood-brain barrier (BBB), which is responsible for maintaining brain homeostasis. This study was aimed to investigate the functional role of microRNA (miR)-132 in hippocampal HT-22 cells under lipopolysaccharide (LPS) stimulation. In vitro cell inflammatory model was constructed by LPS stimulation. Inflammatory cell injury was evaluated according to the alterations of cell viability, apoptosis, and expression of inflammatory cytokines. Then, miR-132 level after LPS treatment was assessed. Subsequently, miR-132 was abnormally expressed after cell transfection, and the effects of miR-132 on LPS-induced cell inflammatory injury as well as phosphorylated levels of key kinases in the NF-κB and MAPK kinase (MEK)/ERK pathways were determined. The target gene of miR-132 was virtually screened and verified, and whether miR-132 affected HT-22 cells under LPS stimulation through regulating the target gene was verified. The results showed that the level of miR-132 was down-regulated by LPS in HT-22 cells, and the LPS-induced inflammatory injury could be reduced by miR-132 overexpression. Then, the phosphorylated levels of kinases in the NF-κB and MEK/ERK pathways were decreased by miR-132 overexpression. Tumor necrosis factor receptor-associated factor 6 (TRAF6) was predicted and verified to be a target of miR-132. Moreover, the alterations induced by miR-132 overexpression in the LPS-treated HT-22 cells were abrogated by TRAF6 overexpression. Therefore, we drew the conclusion that LPS down-regulated miR-132 and miR-132 attenuated LPS-induced inflammatory cell injury by targeting TRAF6, along with the inhibition of the NF-κB and MEK/ERK pathways.

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confidence: 99%

Retracted: MicroRNA‐132 attenuates LPS‐induced inflammatory injury by targeting TRAF6 in neuronal cell line HT‐22

Wang

Liu

et al. 2018

J of Cellular Biochemistry

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“…Zahlreiche Studien bestätigen, dass bei Lebererkrankungen ebenfalls Entzündungsmechanismen im Gehirn auftreten [60][61][62][63][64][65][66]. Bereits seit langen bekannt ist die bei schwerer Leberfunktionsstörung auftretende hepatische Enzephalopathie.…”

Section: Neuroinflammation Durch Lebererkrankungenunclassified

Depressionen und Lebererkrankungen: Die Rolle von Mikrobiom und Inflammation

Kahl

Krüger

Eckermann³

et al. 2018

Fortschr Neurol Psychiatr

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Depression and liver disease are closely associated. Every third patient with liver cirrhosis or hepatitis shows depressive symptoms. On the other hand, every third patient with depressive disorder develops an alcohol disorder at some point during his / her life. A crucial link between depression and hepatic disease seems to be inflammatory processes in which the microbiome and increased intestinal permeability of the intestine play a pivotal role. Depression as well as liver disease, alcohol consumption, stress, and aging processes disturb the delicate balance of intestinal microbiota resulting in increased intestinal permeability. Therefore, bacteria or their metabolites such as the endotoxine lipopolysaccharide are able to reach the blood circulation resulting in inflammation in the liver as well as in the brain via a cytokine cascade, which in turn can lead to liver changes, depression, obesity, and metabolic syndrome. Therefore, liver values, blood glucose levels, and metabolic parameters should be closely monitored in patients with depressive disorders, and in the case of patients with hepatic diseases, increased attention should be given to depressive symptoms, diabetes and obesity.

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“…Before we discuss the key role of metzincins in the modulation of Aβ transport and clearance, we briefly describe the functioning of the main CNS barriers under physiological and pathological conditions. The BBB, BCSFB, and arachnoid barrier are dynamic complexes that maintain brain homeostasis, detect changes in CSF or blood, and provide balanced microenvironments that are critical for protecting the CNS from damage (Abbott et al, 2010; Redzic, 2011; de Wit et al, 2016). The BBB and BCSFB have the largest surface interface between blood and brain extracellular fluids.…”

Section: Expression Of Metzincins In Alzheimer’s Diseasementioning

confidence: 99%

Multifaceted Roles of Metzincins in CNS Physiology and Pathology: From Synaptic Plasticity and Cognition to Neurodegenerative Disorders

Brzdąk

Nowak

Wiera

et al. 2017

Front. Cell. Neurosci.

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The extracellular matrix (ECM) and membrane proteolysis play a key role in structural and functional synaptic plasticity associated with development and learning. A growing body of evidence underscores the multifaceted role of members of the metzincin superfamily, including metalloproteinases (MMPs), A Disintegrin and Metalloproteinases (ADAMs), A Disintegrin and Metalloproteinase with Thrombospondin Motifs (ADAMTSs) and astacins in physiological and pathological processes in the central nervous system (CNS). The expression and activity of metzincins are strictly controlled at different levels (e.g., through the regulation of translation, limited activation in the extracellular space, the binding of endogenous inhibitors and interactions with other proteins). Thus, unsurprising is that the dysregulation of proteolytic activity, especially the greater expression and activation of metzincins, is associated with neurodegenerative disorders that are considered synaptopathies, especially Alzheimer’s disease (AD). We review current knowledge of the functions of metzincins in the development of AD, mainly the proteolytic processing of amyloid precursor protein, the degradation of amyloid β (Aβ) peptide and several pathways for Aβ clearance across brain barriers (i.e., blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB)) that contain specific receptors that mediate the uptake of Aβ peptide. Controlling the proteolytic activity of metzincins in Aβ-induced pathological changes in AD patients’ brains may be a promising therapeutic strategy.

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Inflammation at the blood-brain barrier: The role of liver X receptors

Cited by 24 publications

References 112 publications

Retracted: MicroRNA‐132 attenuates LPS‐induced inflammatory injury by targeting TRAF6 in neuronal cell line HT‐22

Retracted: MicroRNA‐132 attenuates LPS‐induced inflammatory injury by targeting TRAF6 in neuronal cell line HT‐22

Depressionen und Lebererkrankungen: Die Rolle von Mikrobiom und Inflammation

Multifaceted Roles of Metzincins in CNS Physiology and Pathology: From Synaptic Plasticity and Cognition to Neurodegenerative Disorders

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